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University of Sydney
1.
Liang, Christina Luh-Unn.
The Australian Mitochondrial Disease Study – Recognising and improving the diagnosis and management outcomes of adult patients with mitochondrial diseases
.
Degree: 2016, University of Sydney
URL: http://hdl.handle.net/2123/16723 
► Background: Mitochondrial diseases are one of the most common hereditary neuromuscular conditions. Late-onset presentations are common. Genotype-phenotype correlations are poor, making the diagnosis difficult and…
(more)
▼ Background: Mitochondrial diseases are one of the most common hereditary neuromuscular conditions. Late-onset presentations are common. Genotype-phenotype correlations are poor, making the diagnosis difficult and prognostication imprecise. Objectives: We aim to refine the diagnostic pathway for adult patients suspected to have a mitochondrial disease, to better understand their clinical presentations, and to review their management strategies. Methods: At the Neurogenetics Clinic, we saw over 270 patients with suspected mitochondrial disease, of whom 148 patients had “probable” or “definite” disease. To review their most common and distinctive features, we set up a database to collate data on their clinical and investigational findings. Patients presenting with symptoms consistent with POLG1 mutations were screened by direct whole gene sequencing. We report cases of diagnostic challenge and interest. We explored for new diagnostic biomarkers, and devised a prediagnostic screening scale. We audited the patients who required critical care admissions. Results: We identified common pitfalls in diagnosing mitochondrial disease in adult patients, and proposed a new diagnostic paradigm. Among our cohort with features suggestive of POLG-related syndromes, only 10% had pathogenic mutations. We explored the use of FGF-21 (elevated in patients with muscle-manifesting mitochondrial disease); and GDF-15 (indicative of mitochondrial diseases more broadly), and both had significantly greater sensitivity and specificity than traditional blood biomarkers of disease. We created the MitoScale which as a screening tool, has a high sensitivity for the disease. We retrospectively followed a group of critically ill adult patients, and identified the common precipitating events, prodromal symptoms and complications. Conclusion: The diagnostic pathway for patients with suspected mitochondrial disease is improving with next generation genetic sequencing techniques and new serum diagnostic biomarkers. These should be reflected in the revision of diagnostic criteria and screening algorithms. The evidence for patient prognostication and management remains rudimentary, but ongoing research into larger patient cohorts enabled by database networks will help to improve patients’ management outcome.
Subjects/Keywords: Mitochondrial;
Mitochondrial disease;
Database;
Adult
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APA (6th Edition):
Liang, C. L. (2016). The Australian Mitochondrial Disease Study – Recognising and improving the diagnosis and management outcomes of adult patients with mitochondrial diseases
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/16723
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Liang, Christina Luh-Unn. “The Australian Mitochondrial Disease Study – Recognising and improving the diagnosis and management outcomes of adult patients with mitochondrial diseases
.” 2016. Thesis, University of Sydney. Accessed March 08, 2021.
http://hdl.handle.net/2123/16723.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Liang, Christina Luh-Unn. “The Australian Mitochondrial Disease Study – Recognising and improving the diagnosis and management outcomes of adult patients with mitochondrial diseases
.” 2016. Web. 08 Mar 2021.
Vancouver:
Liang CL. The Australian Mitochondrial Disease Study – Recognising and improving the diagnosis and management outcomes of adult patients with mitochondrial diseases
. [Internet] [Thesis]. University of Sydney; 2016. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/2123/16723.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Liang CL. The Australian Mitochondrial Disease Study – Recognising and improving the diagnosis and management outcomes of adult patients with mitochondrial diseases
. [Thesis]. University of Sydney; 2016. Available from: http://hdl.handle.net/2123/16723
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Manitoba
2.
Osman, Fadumo.
DNA methylation mark in mitochondrial DNA.
Degree: Biochemistry and Medical Genetics, 2020, University of Manitoba
URL: http://hdl.handle.net/1993/34630
► DNA methylation, 5-methylcytosine (5-mC), is a key epigenetic modification involved in gene regulation found in the nuclear genome of various organisms. Interestingly, mitochondrial DNA (mtDNA)…
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▼ DNA methylation, 5-methylcytosine (5-mC), is a key epigenetic modification involved in gene regulation found in the nuclear genome of various organisms. Interestingly,
mitochondrial DNA (mtDNA) has also been found to be modified by 5-mC. Research to determine the functional relevance and identify players regulating mtDNA methylation is receiving an ever-increasing interest.
This project is focused on understanding the
mitochondrial methylation patterns in the normal physiological state using circulating CD4+ and CD8+ T cells as an informative study model. This knowledge might prove useful in understanding what arises during the pathological state. Moreover, mtDNA cellular content differs across tissue types depending on several factors including cellular energy demand which influence mtDNA replication and transcription rate. The objective of this study is to determine variations in mtDNA methylation of CD4+ and CD8+ T cells between healthy individuals as well as the ratio of
mitochondrial/nuclear DNA in these cells to estimate whether the changes in methylation could possibly be contributed to changes in their relative mtDNA content.
In this study, blood samples from healthy donors were collected and CD4+ and CD8+ T cells were purified for analyses of 5-mC. The methylated DNA fragments enriched by methyl-CpG binding domain were sequenced and subsequent bioinformatic analysis involved preprocessing of the raw data, alignment of reads to the human
mitochondrial genome and methylation peak calling. Methylation levels within the
mitochondrial D-loop were then quantitatively evaluated by bisulfite-pyrosequencing. The results showed variations in the distribution of 5-mC in the different cell types and individuals, with the exception of 3’ end in the terminal part of D-loop which appeared to be consistently methylated to a certain extent across mtDNA with the average methylation level of ~ 1%. Additionally, quantitative PCR used to measure the ratio of
mitochondrial/nuclear DNA showed no association between mtDNA methylation patterns and their relative mtDNA content. Overall, the low mtDNA methylation level detected deems it unlikely to have a major impact on
mitochondrial function. Nevertheless, it is important to build on this knowledge, know the extent of mtDNA methylation in various cell types and design more comprehensive experiments to prove its biological significance.
Advisors/Committee Members: Davie, James (Biochemistry and Medical Genetics) (supervisor), Leygue, Etienne (Biochemistry and Medical Genetics).
Subjects/Keywords: Mitochondrial epigenetics
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APA (6th Edition):
Osman, F. (2020). DNA methylation mark in mitochondrial DNA. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/34630
Chicago Manual of Style (16th Edition):
Osman, Fadumo. “DNA methylation mark in mitochondrial DNA.” 2020. Masters Thesis, University of Manitoba. Accessed March 08, 2021.
http://hdl.handle.net/1993/34630.
MLA Handbook (7th Edition):
Osman, Fadumo. “DNA methylation mark in mitochondrial DNA.” 2020. Web. 08 Mar 2021.
Vancouver:
Osman F. DNA methylation mark in mitochondrial DNA. [Internet] [Masters thesis]. University of Manitoba; 2020. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/1993/34630.
Council of Science Editors:
Osman F. DNA methylation mark in mitochondrial DNA. [Masters Thesis]. University of Manitoba; 2020. Available from: http://hdl.handle.net/1993/34630
University of Missouri – Columbia
3.
Song, Won-Hee.
Autophagy and ubiquitin-proteasome system during post-fertilization sperm mitophagy.
Degree: 2016, University of Missouri – Columbia
URL: http://hdl.handle.net/10355/62521
► [ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Maternal inheritance of mitochondria and mitochondrial DNA (mtDNA) is a universal principle in developmental biology.…
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▼ [ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Maternal inheritance of mitochondria and
mitochondrial DNA (mtDNA) is a universal principle in developmental biology. Mammalian sperm-borne mitochondria are selectively degraded inside the fertilized oocyte. Our early observations established that post-fertilization degradation of sperm mitochondria is mediated by ubiquitin-proteasome system (UPS), the major protein-turnover pathway that degrades proteins one molecule at a time. Others' recent studies suggested that a whole organelle sperm mitochondrion is degraded by autophagic pathway, which is referred to as sperm mitophagy. Based on this understanding, the first objective of this dissertation was to identify UPS determinants present in porcine sperm mitochondria. The second objective was to characterize the UPS-controlled porcine ooplasmic autophagy receptors that may regulate sperm mitophagy after fertilization. The interaction between UPS and autophagic pathway was revealed during post-fertilization sperm mitophagy. It was determined that the ooplasmic, ubiquitin-binding autophagy receptor SQSTM1 binds to ubiquitinated
mitochondrial membrane proteins, targeting whole mitochondria towards autophagosome. Concurrently, protein dislocase VCP extracts ubiquitinated
mitochondrial membrane proteins and transport them to proteasome. Collectively, these studies offer insight into the mechanisms guiding sperm mitochondrion recognition and disposal after fertilization, which assure normal preimplantation development and prevent a potentially detrimental effect of heteroplasmy.
Advisors/Committee Members: Sutovsky, Peter (advisor).
Subjects/Keywords: Mitochondrial DNA
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APA ·
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APA (6th Edition):
Song, W. (2016). Autophagy and ubiquitin-proteasome system during post-fertilization sperm mitophagy. (Thesis). University of Missouri – Columbia. Retrieved from http://hdl.handle.net/10355/62521
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Song, Won-Hee. “Autophagy and ubiquitin-proteasome system during post-fertilization sperm mitophagy.” 2016. Thesis, University of Missouri – Columbia. Accessed March 08, 2021.
http://hdl.handle.net/10355/62521.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Song, Won-Hee. “Autophagy and ubiquitin-proteasome system during post-fertilization sperm mitophagy.” 2016. Web. 08 Mar 2021.
Vancouver:
Song W. Autophagy and ubiquitin-proteasome system during post-fertilization sperm mitophagy. [Internet] [Thesis]. University of Missouri – Columbia; 2016. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/10355/62521.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Song W. Autophagy and ubiquitin-proteasome system during post-fertilization sperm mitophagy. [Thesis]. University of Missouri – Columbia; 2016. Available from: http://hdl.handle.net/10355/62521
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
4.
김, 영화.
Regulation of Mitochondrial Morphology by ERK1/2-Mediated Control of Mfn2 Stability.
Degree: 2011, Ajou University
URL: http://repository.ajou.ac.kr/handle/201003/4420
;
http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000011940
► 미토콘드리아는 세포 내 에너지 생산뿐만 아니라 세포의 삶과 죽음을 포함한 세포의 운명 결정과 직결된 다양한 생명활동에 관여하고 있으며, 미토콘드리아의 형태(morphology) 조절이 세포의 항상성(homeostasis) 유지에 필수적이라는…
(more)
▼ 미토콘드리아는 세포 내 에너지 생산뿐만 아니라 세포의 삶과 죽음을 포함한 세포의 운명 결정과 직결된 다양한 생명활동에 관여하고 있으며, 미토콘드리아의 형태(morphology) 조절이 세포의 항상성(homeostasis) 유지에 필수적이라는 사실이 차츰 밝혀지고 있다. 미토콘드리아의 형태는 Mitofusin 1(Mfn1), Mitofusin 2(Mfn2), Optic atrophy protein 1(Opa1), Dynamin related protein 1(Drp1), Fission protein 1(Fis1) 등의 미토콘드리아 형태조절 단백질(mitochondria-shaping protein)이 관여하는 미토콘드리아 융합-분열 기구(mitochondrial fusion-fission machinery)에 의해 정교하게 조절되고 있다. 이러한 형태조절 단백질들이 어떻게 분자 수준에서 조절 되어 그들의 역할을 수행하는지에 관해서는 아직 명확하지 않다.
본 연구는 동일한 종류의 primary 배양세포에서ERK1/2의 활성화 정도에 비례하여 미토콘드리아가 짧아지는 현상의 발견으로부터 연구를 시작하게 되었다. ERK1/2는 외부의 다양한 자극에 반응하여 세포성장, 증식, 분화 및 세포의 생(生)과 사(死)를 조절하는 세포 내 필수 kinase 로 최근의 연구에서 ERK1/2가 미토콘드리아 외 막과 내막에 모두 국재(localization) 한다고 보고되었다. 이는 ERK1/2에 의한 신호전달과 미토콘드리아 간에 직접적인 상관관계가 있음을 시사한다.
따라서, 본 연구에서는 ERK1/2의 활성화와 미토콘드리아 형태조절과의 상관관계 규명을 연구목표로 하였다. 우선, ERK1/2활성을 저해 시켜서 미토콘드리아 형태에 미치는 영향을 관찰 하여 ERK1/2의 활성화와 미토콘드리아 형태조절간의 연관성을 확인해 보았다. 여러 종류의 세포에MEK/ERK 특이적 저해제인 PD98059를 처리하여 ERK1/2의 활성을 억제한 결과, 시험한 모든 세포에서 미토콘드리아가 길어지는 것을 확인 하였다. 이러한 ERK1/2의 활성 저해에 의한 미토콘드리아의 형태변화가 미토콘드리아 형태조절 단백질과 직접적으로 연관되어 있는지 분석한 결과, 미토콘드리아 융합(fusion)조절에 관여하는 Mfn2단백질의 특이적 증가를 확인하였다. 다음으로, ERK1/2활성 저해에 의해 Mfn2가 증가된 원인을 밝히기 위한 실험을 진행하였다. Mfn2의 증가가 mRNA 수준에서 유전자 발현(expression)의 증가에 의한 것인지 RT-PCR방법으로 확인하였고, 또한 Mfn2의 증가가 단백질 수준의 안정성(stability) 증가에 의한 것인지 단백질 분해 경로에 관여하는 유비퀴틴화(ubiquitination) 분석을 통하여 확인하였다. 결과적으로 PD98059처리에 의한 ERK1/2의 활성 저해는 유비퀴틴화 감소로 인한 Mfn2 단백질 수준의 안정성을 증가시킨다는 사실을 확인하였다. Mfn2의 유비퀴틴화 감소 원인을 확인 하기 위하여 지금까지 Mfn2의 유비퀴틴화에 관여하는 것으로 보고된 2 종류의 E3 ubiquitin ligase인 MARCH-V와 Parkin을 분석한 결과, PD98059처리에 의한 ERK1/2 활성 저해는 MARCH-V의 발현 감소를 유도 한다는 중요한 사실을 밝혔으며, 이는 MARCH-V의 발현 감소가 Mfn2의 유비퀴틴화 감소에 영향을 미쳤음을 시사한다.
결론적으로, ERK1/2의 활성 변화는 E3 ubiqiutin ligase인 MARCH-V의 발현 량에 영향을 미치고, 이로 인해 미토콘드리아 형태조절 단백질 Mfn2의 안정성의 변화를 가져와 결과적으로 미토콘드리아의 형태 변화를 초래한다는 사실을 밝혔다. 본 연구 결과는 세포의 항상성 유지에 필수적이라고 알려진 미토콘드리아의 형태조절이 ERK1/2 신호전달 경로에 의해 조절되고, 그 균형이 유지되고 있음을 시사한다. 본 연구는 미토콘드리아 형태조절에 의해 매개 되는 다양한 생명현상의 이해 증진에 기여 할 것으로 생각된다.
국문요약 =ⅰ
차례 =ⅳ
그림차례 =ⅴ
표차례 =ⅶ
Ⅰ. 서론 =1
Ⅱ. 재료 및 방법 = 6
A. Cell culture= 6
B. Reagent treatment and Western blot analysis = 6
C. Ras activation assay = 7
D. Mitochondria fractionation = 7
E. Total RNA extraction and cDNA synthesis = 8
F. RT-PCR = 9
G. Immunoprecipitation analysis = 11
H. Confocal microscopy = 11
Ⅲ. 결과 = 13
Ⅳ. 고찰 = 29
Ⅴ. 결론 = 33
참고문헌 = 34
ABSTRACT = 36
Master
Advisors/Committee Members: 대학원 의생명과학과, 200924337, 김, 영화.
Subjects/Keywords: Mitochondrial; ERK1/2; Mitochondrial morphology; 미토콘드리아
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APA ·
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APA (6th Edition):
김, . (2011). Regulation of Mitochondrial Morphology by ERK1/2-Mediated Control of Mfn2 Stability. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/4420 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000011940
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
김, 영화. “Regulation of Mitochondrial Morphology by ERK1/2-Mediated Control of Mfn2 Stability.” 2011. Thesis, Ajou University. Accessed March 08, 2021.
http://repository.ajou.ac.kr/handle/201003/4420 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000011940.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
김, 영화. “Regulation of Mitochondrial Morphology by ERK1/2-Mediated Control of Mfn2 Stability.” 2011. Web. 08 Mar 2021.
Vancouver:
김 . Regulation of Mitochondrial Morphology by ERK1/2-Mediated Control of Mfn2 Stability. [Internet] [Thesis]. Ajou University; 2011. [cited 2021 Mar 08].
Available from: http://repository.ajou.ac.kr/handle/201003/4420 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000011940.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
김 . Regulation of Mitochondrial Morphology by ERK1/2-Mediated Control of Mfn2 Stability. [Thesis]. Ajou University; 2011. Available from: http://repository.ajou.ac.kr/handle/201003/4420 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000011940
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
5.
Berg Alonso, Laetitia.
Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes : Non communiqué.
Degree: Docteur es, Interactions moléculaires et cellulaires, 2016, Université Côte d'Azur (ComUE)
URL: http://www.theses.fr/2016AZUR4101
► Les maladies mitochondriales regroupent un ensemble de pathologies liées à un déficit de la chaînerespiratoire mitochondriale. Au laboratoire, nous focalisons notre intérêt sur les mitochondriopathies…
(more)
▼ Les maladies mitochondriales regroupent un ensemble de pathologies liées à un déficit de la chaînerespiratoire mitochondriale. Au laboratoire, nous focalisons notre intérêt sur les mitochondriopathies liées à undéfaut de stabilité de l’ADN mitochondrial (ADNmt), qui se traduit par des délétions multiples et/ou unedéplétion (diminution du nombre de copies). Ces pathologies sont caractérisées par une importantehétérogénéité clinique et génétique et sont secondaires à des mutations dans des gènes nucléaires codantpour des protéines impliquées dans le maintien de l’ADNmt. De nos jours, la recherche des gènesresponsables d’instabilité de l’ADNmt s’avère négative chez plus de 70% des malades, d’où un grand intérêtpour améliorer les techniques d’identification des mutations et la recherche de nouveaux gènes impliquésdans ces pathologies
Non communiqué
Advisors/Committee Members: Paquis-Fluckinger, Véronique (thesis director).
Subjects/Keywords: Maladie mitochondriale; ADNmt; Mitochondrial disease; Mitochondrial DNA
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APA ·
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to Zotero / EndNote / Reference
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APA (6th Edition):
Berg Alonso, L. (2016). Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes : Non communiqué. (Doctoral Dissertation). Université Côte d'Azur (ComUE). Retrieved from http://www.theses.fr/2016AZUR4101
Chicago Manual of Style (16th Edition):
Berg Alonso, Laetitia. “Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes : Non communiqué.” 2016. Doctoral Dissertation, Université Côte d'Azur (ComUE). Accessed March 08, 2021.
http://www.theses.fr/2016AZUR4101.
MLA Handbook (7th Edition):
Berg Alonso, Laetitia. “Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes : Non communiqué.” 2016. Web. 08 Mar 2021.
Vancouver:
Berg Alonso L. Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes : Non communiqué. [Internet] [Doctoral dissertation]. Université Côte d'Azur (ComUE); 2016. [cited 2021 Mar 08].
Available from: http://www.theses.fr/2016AZUR4101.
Council of Science Editors:
Berg Alonso L. Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes : Non communiqué. [Doctoral Dissertation]. Université Côte d'Azur (ComUE); 2016. Available from: http://www.theses.fr/2016AZUR4101
University of Utah
6.
Karren, Mary Anne.
Mechanisms of Dnm1p-mediated mitochondrial fission.
Degree: PhD, Biochemistry;, 2007, University of Utah
URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/26/rec/747
► Mitochondria are semiautonomous organelles essential for eukaryotic life. Mitochondria house the machinery required for cellular respiration and energy production, and hundreds of enzymes required for…
(more)
▼ Mitochondria are semiautonomous organelles essential for eukaryotic life. Mitochondria house the machinery required for cellular respiration and energy production, and hundreds of enzymes required for essential biochemical pathways. Mitochondrial number and distribution are regulated by coordinated mitochondrial fission, fusion, and movement events, and must continually adapt to meet the changing spatial and temporal energy requirements of growing cells. In recent years, it has become clear that defects in mitochondrial fission, fusion, or movement can lead to cellular dysfunction and disease. This dissertation investigates the molecular basis for the process of mitochondrial fission in the budding yeast, Saccharomyces cerevisiae . Mitochondrial fission is mediated by macromolecular protein complexes localized to the cytoplasmic face of the outer mitochondrial membrane. These complexes are composed of at least three components, Dnm1p, Fis1p, and Mdv1p. Studies presented in this dissertation investigate the coordinated series of inter- and intramolecular interactions required to recruit and assemble these three proteins into functional fission complexes. Studies detailed in Chapter 2 suggest that the cytoplasmic domain of Fis1p interacts directly with Mdv1p, and that this interaction is required for the recruitment of Dnm1p to functional fission complexes. Results presented in Chapter 3 demonstrate that dimeric Dnm1p is initially recruited to mitochondria, and that higher-ordered Dnm1p oligomerization occurs after mitochondrial recruitment. In addition, Chapter 3 suggests that GTP hydrolysis by Dnm1p is required to destabilize mitochondrial fission complexes after fission occurs. Analyses presented in Chapter 4 characterize the domain of Dnm1p required for Dnm1p association with the actin cytoskeleton. Together, these studies comprise a significant advance in our understanding of the molecular basis for mitochondrial fission, and raise important issues for future study.
Subjects/Keywords: Genetics; DNA, Mitochondrial
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APA (6th Edition):
Karren, M. A. (2007). Mechanisms of Dnm1p-mediated mitochondrial fission. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/26/rec/747
Chicago Manual of Style (16th Edition):
Karren, Mary Anne. “Mechanisms of Dnm1p-mediated mitochondrial fission.” 2007. Doctoral Dissertation, University of Utah. Accessed March 08, 2021.
http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/26/rec/747.
MLA Handbook (7th Edition):
Karren, Mary Anne. “Mechanisms of Dnm1p-mediated mitochondrial fission.” 2007. Web. 08 Mar 2021.
Vancouver:
Karren MA. Mechanisms of Dnm1p-mediated mitochondrial fission. [Internet] [Doctoral dissertation]. University of Utah; 2007. [cited 2021 Mar 08].
Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/26/rec/747.
Council of Science Editors:
Karren MA. Mechanisms of Dnm1p-mediated mitochondrial fission. [Doctoral Dissertation]. University of Utah; 2007. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/26/rec/747
Mississippi State University
7.
Xiao, Ningyu.
Genetic insight into the function of Pcp1p, a mitochondrial rhomboid protease.
Degree: MS, Biological Sciences, 2013, Mississippi State University
URL: http://sun.library.msstate.edu/ETD-db/theses/available/etd-02282013-190211/
;
► Rhomboid peptidases are conserved intramembrane serine proteases with mitochondrial family members being involved in mitochondrial dynamics and apoptosis. The <i>Saccharomyces cerevisiae</i> mitochondrial rhomboid, Pcp1p,…
(more)
▼ Rhomboid peptidases are conserved intramembrane serine proteases with
mitochondrial family members being involved in
mitochondrial dynamics and apoptosis. The <i>Saccharomyces cerevisiae</i>
mitochondrial rhomboid, Pcp1p, catalyzes the cleavage of two substrates: Ccp1p, which breaks down reactive oxygen species, and Mgm1p, a GTPase mediating
mitochondrial fusion events. As an initial approach to determine the structural basis of Pcp1p activity, a screen to identify temperature sensitive alleles of <i>PCP1</i> was performed using hydroxylamine mutagenesis. Eight mutants were identified from a pool of 30,000 colonies that exhibited either temperature sensitive growth or respiratory defects. These mutants also exhibited defects in Mgm1p and Ccp1p processing and some degree of abnormal
mitochondrial morphology. The majority of amino acid changes occurred within the fourth and sixth transmembrane domains of Pcp1p, the location of the active site serine and histidine residues, supporting a role for these transmembrane helices in Pcp1p activity.
Advisors/Committee Members: Donna M. Gordon (chair).
Subjects/Keywords: mitochondrial rhomboid; Pcp1p
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APA (6th Edition):
Xiao, N. (2013). Genetic insight into the function of Pcp1p, a mitochondrial rhomboid protease. (Masters Thesis). Mississippi State University. Retrieved from http://sun.library.msstate.edu/ETD-db/theses/available/etd-02282013-190211/ ;
Chicago Manual of Style (16th Edition):
Xiao, Ningyu. “Genetic insight into the function of Pcp1p, a mitochondrial rhomboid protease.” 2013. Masters Thesis, Mississippi State University. Accessed March 08, 2021.
http://sun.library.msstate.edu/ETD-db/theses/available/etd-02282013-190211/ ;.
MLA Handbook (7th Edition):
Xiao, Ningyu. “Genetic insight into the function of Pcp1p, a mitochondrial rhomboid protease.” 2013. Web. 08 Mar 2021.
Vancouver:
Xiao N. Genetic insight into the function of Pcp1p, a mitochondrial rhomboid protease. [Internet] [Masters thesis]. Mississippi State University; 2013. [cited 2021 Mar 08].
Available from: http://sun.library.msstate.edu/ETD-db/theses/available/etd-02282013-190211/ ;.
Council of Science Editors:
Xiao N. Genetic insight into the function of Pcp1p, a mitochondrial rhomboid protease. [Masters Thesis]. Mississippi State University; 2013. Available from: http://sun.library.msstate.edu/ETD-db/theses/available/etd-02282013-190211/ ;
Vanderbilt University
8.
Clay, Hayley Boyd.
Roles of the mitochondrial fatty acid synthesis II (mtFASII) pathway in mitochondrial function and signaling.
Degree: PhD, Neuroscience, 2016, Vanderbilt University
URL: http://hdl.handle.net/1803/12339
► Despite the presence of a cytosolic fatty acid synthesis pathway, mitochondria have retained their own means of creating fatty acids via the mitochondrial fatty acid…
(more)
▼ Despite the presence of a cytosolic fatty acid synthesis pathway, mitochondria have retained their own means of creating fatty acids via the
mitochondrial fatty acid synthesis (mtFASII) pathway. The reason for its conservation has not yet been elucidated. Therefore, to better understand the role of mtFASII in the cell, we used a variety of methods to characterize the consequences of changes in mtFASII functionality in whole cells, isolated mitochondria, and
mitochondrial secretions. We altered mtFASII functionality by knockdown of acyl carrier protein (ACP) or overexpression of
mitochondrial trans-2-enoyl-CoA reductase (MECR). As a control for known respiratory deficits in mtFASII knockdowns, we also knocked down a component of complex I of the electron transport chain. We found that loss of mtFASII function disturbs metabolism and bioactive lipid regulation at the whole-cell and
mitochondrial levels. We found that the
mitochondrial secretome may contain bioactive lipids and small peptides, and that knockdown of the mtFASII pathway results in increased levels of dipeptides, among other metabolites, in the
mitochondrial secretome. These data indicate that the mtFASII pathway may have a role in
mitochondrial signaling in a manner not linked to mtFASII’s effects on the electron transport chain.
Advisors/Committee Members: Deborah Murdock (committee member), Sandra Zinkel (committee member), Laura Dugan (committee member), Bruce Carter (committee member), Aaron Bowman (Committee Chair).
Subjects/Keywords: mitochondrial signaling; metabolomics
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APA (6th Edition):
Clay, H. B. (2016). Roles of the mitochondrial fatty acid synthesis II (mtFASII) pathway in mitochondrial function and signaling. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/12339
Chicago Manual of Style (16th Edition):
Clay, Hayley Boyd. “Roles of the mitochondrial fatty acid synthesis II (mtFASII) pathway in mitochondrial function and signaling.” 2016. Doctoral Dissertation, Vanderbilt University. Accessed March 08, 2021.
http://hdl.handle.net/1803/12339.
MLA Handbook (7th Edition):
Clay, Hayley Boyd. “Roles of the mitochondrial fatty acid synthesis II (mtFASII) pathway in mitochondrial function and signaling.” 2016. Web. 08 Mar 2021.
Vancouver:
Clay HB. Roles of the mitochondrial fatty acid synthesis II (mtFASII) pathway in mitochondrial function and signaling. [Internet] [Doctoral dissertation]. Vanderbilt University; 2016. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/1803/12339.
Council of Science Editors:
Clay HB. Roles of the mitochondrial fatty acid synthesis II (mtFASII) pathway in mitochondrial function and signaling. [Doctoral Dissertation]. Vanderbilt University; 2016. Available from: http://hdl.handle.net/1803/12339
University of Hawaii – Manoa
9.
Juan, Jemily Gamiao.
Systemic mitochondrial function, type 2 diabetes, obesity, and life-style modifications.
Degree: 2016, University of Hawaii – Manoa
URL: http://hdl.handle.net/10125/100875
► M.S. University of Hawaii at Manoa 2012.
Mitochondrial (mt) dysfunction is emerging as a key factor of T2DM. We hypothesize that systemic mt function in…
(more)
▼ M.S. University of Hawaii at Manoa 2012.
Mitochondrial (mt) dysfunction is emerging as a key factor of T2DM. We hypothesize that systemic mt function in PBMCs is altered in the presence of T2DM and obesity, and can be improved with life-style modifications, regardless of T2DM and obesity status.
In a cross-sectional study (N = 84), PBMC mtDNA levels and OXPHOS Complex I protein levels are increased in the presence of obesity and decreased in the presence of T2DM. Mt parameters correlated with clinical and metabolic measurements. In a longitudinal study, systemic mt function is increased in PBMCs due to life-style modifications, regardless of T2DM status. Findings in our investigations show that systemic mt function in PBMCs is altered in the presence of T2DM and/or obesity and can be improved with life-style modifications. Our study suggests that altered mt function in PBMCs is associated with T2DM and obesity, and can be improved through life-style modifications.
Subjects/Keywords: mitochondrial dysfunction; T2DM
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APA (6th Edition):
Juan, J. G. (2016). Systemic mitochondrial function, type 2 diabetes, obesity, and life-style modifications. (Thesis). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/100875
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Juan, Jemily Gamiao. “Systemic mitochondrial function, type 2 diabetes, obesity, and life-style modifications.” 2016. Thesis, University of Hawaii – Manoa. Accessed March 08, 2021.
http://hdl.handle.net/10125/100875.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Juan, Jemily Gamiao. “Systemic mitochondrial function, type 2 diabetes, obesity, and life-style modifications.” 2016. Web. 08 Mar 2021.
Vancouver:
Juan JG. Systemic mitochondrial function, type 2 diabetes, obesity, and life-style modifications. [Internet] [Thesis]. University of Hawaii – Manoa; 2016. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/10125/100875.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Juan JG. Systemic mitochondrial function, type 2 diabetes, obesity, and life-style modifications. [Thesis]. University of Hawaii – Manoa; 2016. Available from: http://hdl.handle.net/10125/100875
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Kansas
10.
Roy, Nairita.
INVESTIGATING THE PRESENCE OF MITOCHONDRIAL DNA METHYLATION, ITS ALTERATION AND ASSOCIATION WITH MITOCHONDRIAL TRANSCRIPTION AND MITOCHONDRIAL FUNCTION.
Degree: PhD, Molecular & Integrative Physiology, 2015, University of Kansas
URL: http://hdl.handle.net/1808/21927
► Mitochondrial proteins are encoded by both the nuclear and mitochondrial genome (mtDNA). Thus, alterations in mtDNA affect mitochondrial function and are involved in a plethora…
(more)
▼ Mitochondrial proteins are encoded by both the nuclear and
mitochondrial genome (mtDNA). Thus, alterations in mtDNA affect
mitochondrial function and are involved in a plethora of diseases associated with
mitochondrial dysfunction. Although role of nuclear DNA methylation in regulating gene expression is fairly well understood, the very existence of mtDNA methylation has been debated for the past four decades. In spite of the controversies revolving mtDNA methylation, differences in mtDNA methylation have been reported in a number of pathological conditions. However, role of mtDNA methylation in regulating transcription of mtDNA and consequently,
mitochondrial function remains unexplored. Besides, whether mtDNA methylation can be altered experimentally has not been investigated. The goal of this dissertation is to establish a method to quantitate mtDNA methylation and evaluate its presence in SH-SY5Y neuroblastoma cells; examine if mtDNA methylation can be altered and if there are any associated changes in
mitochondrial transcription and function; and further, determine if mtDNA methylation is altered in a model associated with
mitochondrial dysfunction. In Chapter II, we aimed to investigate the presence of mtDNA methylation in SH-SY5Y neuroblastoma cells at global and site-specific levels. In order to investigate the presence of methylation at global levels in SH-SY5Y mtDNA, we established a direct, sensitive and highly specific method using HPLC-ESI-MS/MS by addressing limitations such as differential or incomplete enzymatic digestion of DNA and also, potential nuclear DNA contamination. Differential enzymatic digestion of DNA was addressed by incorporation of one-step digestion for DNA and using oligonucleotides harboring known amounts of dC and 5m-dC as calibrators. 5m-dC was detected in a linear and proportional manner in SH-SY5Y mtDNA. Around 3% methylation was found in mtDNA obtained from crude
mitochondrial isolates, which was comparable to whole-cell DNA methylation levels. Interestingly, similar percentages of methylation were observed even in mtDNA obtained from gradient-purified mitochondria. Further, purity of mtDNA was characterized, indicating elimination of 99.95 % of nuclear DNA contamination with 115 fold-enrichment of mtDNA in gradient-purified mitochondria. Presence of methylation in SH-SY5Y mtDNA was further substantiated using methylation-specific PCR for a specific site in 12S rRNA. Thus, we established a direct method to quantify global methylation in mtDNA using HPLC-MS/MS and also, reported presence of methylated DNA in purified SH-SY5Y mitochondria. In Chapter III, we investigated if mtDNA methylation can be altered by experimental interventions and whether altered mtDNA methylation has any concomitant effects on
mitochondrial transcription and
mitochondrial function. Global mtDNA methylation was assessed by HPLC-ESI-MS/MS and site-specific methylation of 12S rRNA was studied by methylation-specific PCR assay. DNMT1 is known to localize in mitochondria but its role in mtDNA methylation is…
Advisors/Committee Members: Swerdlow, Russell H. (advisor), Geiger, Paige C. (cmtemember), Welch, Danny R. (cmtemember), Peterson, Kenneth R. (cmtemember), Fontes, Joseph D. (cmtemember).
Subjects/Keywords: Physiology; Biochemistry; Genetics; aging; cytoplasmic hybrids; DNA methylation; Mitochondrial DNA; mitochondrial function; mitochondrial transcription
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APA (6th Edition):
Roy, N. (2015). INVESTIGATING THE PRESENCE OF MITOCHONDRIAL DNA METHYLATION, ITS ALTERATION AND ASSOCIATION WITH MITOCHONDRIAL TRANSCRIPTION AND MITOCHONDRIAL FUNCTION. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/21927
Chicago Manual of Style (16th Edition):
Roy, Nairita. “INVESTIGATING THE PRESENCE OF MITOCHONDRIAL DNA METHYLATION, ITS ALTERATION AND ASSOCIATION WITH MITOCHONDRIAL TRANSCRIPTION AND MITOCHONDRIAL FUNCTION.” 2015. Doctoral Dissertation, University of Kansas. Accessed March 08, 2021.
http://hdl.handle.net/1808/21927.
MLA Handbook (7th Edition):
Roy, Nairita. “INVESTIGATING THE PRESENCE OF MITOCHONDRIAL DNA METHYLATION, ITS ALTERATION AND ASSOCIATION WITH MITOCHONDRIAL TRANSCRIPTION AND MITOCHONDRIAL FUNCTION.” 2015. Web. 08 Mar 2021.
Vancouver:
Roy N. INVESTIGATING THE PRESENCE OF MITOCHONDRIAL DNA METHYLATION, ITS ALTERATION AND ASSOCIATION WITH MITOCHONDRIAL TRANSCRIPTION AND MITOCHONDRIAL FUNCTION. [Internet] [Doctoral dissertation]. University of Kansas; 2015. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/1808/21927.
Council of Science Editors:
Roy N. INVESTIGATING THE PRESENCE OF MITOCHONDRIAL DNA METHYLATION, ITS ALTERATION AND ASSOCIATION WITH MITOCHONDRIAL TRANSCRIPTION AND MITOCHONDRIAL FUNCTION. [Doctoral Dissertation]. University of Kansas; 2015. Available from: http://hdl.handle.net/1808/21927
Oregon State University
11.
Wang, Jing.
Chemical labeling methods and mass spectrometry of mitochondrial thiol proteomes.
Degree: PhD, Chemistry, 2011, Oregon State University
URL: http://hdl.handle.net/1957/21985
► Dysfunction of mitochondria has been linked to aging and the pathogenesis of many degenerative diseases. Aside from their primary function in energy production, mitochondria are…
(more)
▼ Dysfunction of mitochondria has been linked to aging and the pathogenesis of many degenerative diseases. Aside from their primary function in energy production, mitochondria are considered as a major source and target of reactive oxygen and nitrogen species (ROS/RNS) in cells as well. The
mitochondrial thiol proteome is a subset of proteins inside mitochondria particularly vulnerable to oxidative modifications often caused by ROS/RNS due to the high reactivity of thiol groups. In this dissertation, we used chemoselective labeling approaches to target
mitochondrial thiol proteomes with two distinct purposes. In the first part of our study, a mitochondria-targeted cationic sulfhydryl reagent, (4-iodobutyl)triphenyl- phosphonium (IBTP), was used to label the protein thiols. This study was focused on the investigation of the tandem mass spectrometric behaviors of the thiol peptides modified by IBTP. In the latter part of the dissertation, we tested the hypothesis that the thiol proteomes of cardiac mitochondria undergo chemical changes as a consequence of aging. The thiol-reactive isotope-coded affinity tags (ICATs) were utilized to estimate the possible age-related impacts on the relative abundances of protein thiols in two
mitochondrial subpopulations present in rat myocardium, respectively.
Fixed charge chemical modifications on peptides and proteins can have significant effects on the ion fragmentation behaviors in tandem mass spectrometry (MS/MS). The MS/MS fragmentation behavior of butyltriphenylphosphonium (BTP)-modified peptides was evaluated via the comparison to their carbamidomethylated (CAM) analogues using a quadrupole ion trap mass spectrometer (LCQ) and/or a quadrupole time-of-flight (QTOF) instrument under conditions of low energy collision-induced dissociation (CID). Besides the expected higher charge states observed in peptides and fragment ions containing the BTP moiety, the charged BTP group also had a significant effect on the amide bond fragmentation products of modified cysteine-containing peptides. The presence of a phosphonium ion was speculated to reduce the tendency for the protonation of the proximal amide bonds in the peptide backbones, and consequently decrease the product ion abundances at the corresponding cleavage sites when compared to those from the CAM-modified derivatives. This effect was particularly noticeable when an Xxx-Pro bond was in the vicinity of a BTP group. Calculations indicated that proton affinities were generally 20-50 kcal/mol lower for BTP-modified peptides in contrast to the respective unmodified or CAM-modified analogues.
In the latter part of the dissertation, we focused on the evaluation of age-related effects on protein thiol abundances in cardiac subsarcolemmal and interfibrillar mitochondria (SSM/IFM). A total of 243 cysteine residues from 115 proteins in SSM and 149 cysteine sites from 65 proteins in IFM were identified from both young and old rats using ICAT labeling approach, respectively. Significant age-related differences (p-value < 0.05) in…
Advisors/Committee Members: Maier, Claudia S. (advisor), Barofsky, Douglas F. (committee member).
Subjects/Keywords: Mitochondrial Thiol Proteomes; Proteins – Spectra
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APA (6th Edition):
Wang, J. (2011). Chemical labeling methods and mass spectrometry of mitochondrial thiol proteomes. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/21985
Chicago Manual of Style (16th Edition):
Wang, Jing. “Chemical labeling methods and mass spectrometry of mitochondrial thiol proteomes.” 2011. Doctoral Dissertation, Oregon State University. Accessed March 08, 2021.
http://hdl.handle.net/1957/21985.
MLA Handbook (7th Edition):
Wang, Jing. “Chemical labeling methods and mass spectrometry of mitochondrial thiol proteomes.” 2011. Web. 08 Mar 2021.
Vancouver:
Wang J. Chemical labeling methods and mass spectrometry of mitochondrial thiol proteomes. [Internet] [Doctoral dissertation]. Oregon State University; 2011. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/1957/21985.
Council of Science Editors:
Wang J. Chemical labeling methods and mass spectrometry of mitochondrial thiol proteomes. [Doctoral Dissertation]. Oregon State University; 2011. Available from: http://hdl.handle.net/1957/21985
University of Utah
12.
Speyer, Joseph Frederick.
On the mechanism of aconitase.
Degree: PhD, Biochemistry;, 1954, University of Utah
URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/2053/rec/839
► Analysis of aconitase kinetics shows that all three substrates, citrate, d(+)-isocitrate, and cis aconitate, are equivalent in the number of slow, rate determining steps in…
(more)
▼ Analysis of aconitase kinetics shows that all three substrates, citrate, d(+)-isocitrate, and cis aconitate, are equivalent in the number of slow, rate determining steps in their inter-conversion. Kinetics and the inhibition studies using deuterium oxide indicate that cis aconitate is not an obligatory intermediate in the citrate: isocitrate conversion. The lack of deuterium incorporation from the medium into enzymatically formed citrate from isocitrate shows that conversion to involve and intramolecular hydrogen rearrangement and eliminates cis aconitate as the intermediate. The proposed mechanism is similar to known intramolecular hydrogen rearrangements, the Whitmore Shift of carbonium ions; It is though that the enzyme can induce carbonium ion formation in the substrate with the aid of ferrous iron. It is postulated that the metal serves as an electron acceptor or Lewis acid, and that the carbonium ion is formed as a result of coordination of the hydroxyl with the metal. The postulated mechanism accounts for all the reactions of he enzyme and for its kinetic behavior. Aconitase has been prepared from mitochondria by freezing and thawing. The soluble aconitase is more active than the mitochondrial enzyme in the isocitrate-aconitate and citrate-aconitate reactions, but mitochondrial aconitase is more active in the isocitrate-citrate transformation. Soluble aconitase showed an optimum at pH 7.3 but mitochondrial aconitase showed optima at pH 5.8 and 7.3. The isocitrate-aconitate and citrate-aconitate reactions of both soluble and mitochondrial aconitase were inhibited by o-phenanthroline and reactivated by ferrous ions plus ascorbate. Mitochondria incubated with isocitrate retain aconitate. The data on the intracellular distribution of aconitase were markedly affected by the condition of the assay.
Subjects/Keywords: Metabolism; Mitochondrial
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APA (6th Edition):
Speyer, J. F. (1954). On the mechanism of aconitase. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/2053/rec/839
Chicago Manual of Style (16th Edition):
Speyer, Joseph Frederick. “On the mechanism of aconitase.” 1954. Doctoral Dissertation, University of Utah. Accessed March 08, 2021.
http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/2053/rec/839.
MLA Handbook (7th Edition):
Speyer, Joseph Frederick. “On the mechanism of aconitase.” 1954. Web. 08 Mar 2021.
Vancouver:
Speyer JF. On the mechanism of aconitase. [Internet] [Doctoral dissertation]. University of Utah; 1954. [cited 2021 Mar 08].
Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/2053/rec/839.
Council of Science Editors:
Speyer JF. On the mechanism of aconitase. [Doctoral Dissertation]. University of Utah; 1954. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/2053/rec/839
Rochester Institute of Technology
13.
Ruda, Melissa.
A Study of phylogenetic trees versus networks to objectively identify haplogroups in mitochondrial dna.
Degree: Thomas H. Gosnell School of Life Sciences (COS), 2011, Rochester Institute of Technology
URL: https://scholarworks.rit.edu/theses/4109
► Mitochondrial DNA is important in the studies of population, medicine, migration, and forensics, as well as a few other disciplines. Further insight on grouping mtDNA…
(more)
▼ Mitochondrial DNA is important in the studies of population, medicine, migration, and forensics, as well as a few other disciplines. Further insight on grouping mtDNA sequences could give insight on identifying genetic variation that causes susceptibility to disease, more personalized medicines, or more effective forensic analysis.
Mitochondrial DNA is currently grouped into haplogroups determined from phylogenetic tree analysis. Phylogenetic tree analysis may not be the optimal solution for mtDNA because they work better for data above the species level, to show population relationships, not sequences that only differ by a few nucleotides.
To compare both analysis, sample data was obtained from Phylotree.org (van Oven & Kayser, 2009). The sequences were run through Clustal W (Latkin et al., 2007) for a multi sequence alignment. The results were then used to create a Neighbor-Joining phylogenetic tree in PAUP* 4.0 (David Swofford, 1993). The results where then compared to a phylogenetic network created using SplitsTree4 (D. H. Huson and D. Bryant 2006). The groupings in the network were compared to the groupings in the tree as well as what would be expected based on haplogroups. Even though the results were similar, the phylogenetic network did give a slightly more thorough result.
Advisors/Committee Members: Osier, Michael.
Subjects/Keywords: Haplogroups; Mitochondrial DNA; Phylogenetics
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APA (6th Edition):
Ruda, M. (2011). A Study of phylogenetic trees versus networks to objectively identify haplogroups in mitochondrial dna. (Thesis). Rochester Institute of Technology. Retrieved from https://scholarworks.rit.edu/theses/4109
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Ruda, Melissa. “A Study of phylogenetic trees versus networks to objectively identify haplogroups in mitochondrial dna.” 2011. Thesis, Rochester Institute of Technology. Accessed March 08, 2021.
https://scholarworks.rit.edu/theses/4109.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ruda, Melissa. “A Study of phylogenetic trees versus networks to objectively identify haplogroups in mitochondrial dna.” 2011. Web. 08 Mar 2021.
Vancouver:
Ruda M. A Study of phylogenetic trees versus networks to objectively identify haplogroups in mitochondrial dna. [Internet] [Thesis]. Rochester Institute of Technology; 2011. [cited 2021 Mar 08].
Available from: https://scholarworks.rit.edu/theses/4109.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ruda M. A Study of phylogenetic trees versus networks to objectively identify haplogroups in mitochondrial dna. [Thesis]. Rochester Institute of Technology; 2011. Available from: https://scholarworks.rit.edu/theses/4109
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Alberta
14.
Bahitham, Wesam Ahmad.
Novel Alterations of Morphology and Genome of Mitochondria
of Cholangiocellular Carcinoma.
Degree: MS, Medical Sciences- Laboratory Medicine and
Pathology, 2013, University of Alberta
URL: https://era.library.ualberta.ca/files/mc87pq769
► Cholangiocellular carcinoma (CCA) is the second most common hepatic malignancy, but its carcinogenesis is poorly understood. Somatic mitochondrial DNA (mtDNA) mutations have been demonstrated in…
(more)
▼ Cholangiocellular carcinoma (CCA) is the second most
common hepatic malignancy, but its carcinogenesis is poorly
understood. Somatic mitochondrial DNA (mtDNA) mutations have been
demonstrated in a variety of human cancers. However, no study has
previously investigated mitochondria and their genome alterations
in CCA. Our findings suggest that mtDNA alterations are an
important event during the carcinogenesis of CCA. In comparison
with normal cell lines and other liver malignancies, both
morphologic and functional changes of mitochondria and
mitochondrial genome point to a striking result that may play a
major role in the aggressiveness of CCA.
Subjects/Keywords: mtDNA; Cholangiocarcinoma; Mitochondrial dysfunction; MitoChip
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APA (6th Edition):
Bahitham, W. A. (2013). Novel Alterations of Morphology and Genome of Mitochondria
of Cholangiocellular Carcinoma. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/mc87pq769
Chicago Manual of Style (16th Edition):
Bahitham, Wesam Ahmad. “Novel Alterations of Morphology and Genome of Mitochondria
of Cholangiocellular Carcinoma.” 2013. Masters Thesis, University of Alberta. Accessed March 08, 2021.
https://era.library.ualberta.ca/files/mc87pq769.
MLA Handbook (7th Edition):
Bahitham, Wesam Ahmad. “Novel Alterations of Morphology and Genome of Mitochondria
of Cholangiocellular Carcinoma.” 2013. Web. 08 Mar 2021.
Vancouver:
Bahitham WA. Novel Alterations of Morphology and Genome of Mitochondria
of Cholangiocellular Carcinoma. [Internet] [Masters thesis]. University of Alberta; 2013. [cited 2021 Mar 08].
Available from: https://era.library.ualberta.ca/files/mc87pq769.
Council of Science Editors:
Bahitham WA. Novel Alterations of Morphology and Genome of Mitochondria
of Cholangiocellular Carcinoma. [Masters Thesis]. University of Alberta; 2013. Available from: https://era.library.ualberta.ca/files/mc87pq769
Cornell University
15.
Ye, Kaixiong.
The Evolutionary And Clinical Significance Of Regulatory And Mitochondrial Genetic Variants.
Degree: PhD, Nutrition, 2015, Cornell University
URL: http://hdl.handle.net/1813/39371
► Genetic adaptations to local environment during evolution shaped the human genome. Identifying evolutionarily important genetic variants is clinically significant because the mismatch between our slow-evolving…
(more)
▼ Genetic adaptations to local environment during evolution shaped the human genome. Identifying evolutionarily important genetic variants is clinically significant because the mismatch between our slow-evolving genome and the cultural upheaval underlies many diseases of civilization. Recent sequencing technology advances start a Genomic era and promise to elucidate the genetic basis of human health and disease. While most attention had been drawn to protein-coding genes in the nuclear genome, regulatory regions and
mitochondrial genome were much less studied. My research aims to investigate the evolutionary and clinical significance of these two categories. Starting my research, I summarized the latest advances in understanding the role of nutrition in human genome evolution and introduced to the Nutrition field population genomics approaches to identify dietary adaptions. My first research project examined the adaptation of regulatory variants to 42 environmental factors. With a newly developed environmental correlation method, I found that expression QTLs are enriched in signals of environmental adaptation and regulatory adaptation are especially important for some environmental factors, like climate, and for some biological pathways, including immune and metabolic pathways. My second project was a case study to test a hypothesis that an Asian-common haplotype was adaptive to the plant-based diet in Asia by enhancing non-heme iron absorption. With an iron absorption study involving 57 Asian women volunteers, I found that consistent to our hypothesis homozygous carriers of the adaptive haplotype absorbed 22% more non-heme iron than non-carriers. Intriguingly, I also observed that compared to Caucasian women, Asian women absorbed more non-heme iron even in face of higher iron store. My third project utilized the next-generation sequencing data from the 1000 Genomes Project and investigated the prevalence and clinical relevance of
mitochondrial DNA (mtDNA) heteroplasmy, the presence of multiple versions of mtDNA in a cell. I found that about 90% healthy individuals carry at least one heteroplasmies and at least 20% individuals harbor disease-associated heteroplasmies. I demonstrated that heteroplasmic mutations are highly pathogenic and
subject to weak negative selection. My research suggests that heteroplasmic mutations may drift to high frequency across life-span and contribute to age-related diseases.
Advisors/Committee Members: Gu, Zhenglong (chair), Booth, James (committee member), Mezey, Jason G. (committee member), O'Brien, Kimberly O (committee member), Brenna, James Thomas (committee member).
Subjects/Keywords: Adaptation; Regulatory Variants; Mitochondrial Heteroplasmy
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APA (6th Edition):
Ye, K. (2015). The Evolutionary And Clinical Significance Of Regulatory And Mitochondrial Genetic Variants. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/39371
Chicago Manual of Style (16th Edition):
Ye, Kaixiong. “The Evolutionary And Clinical Significance Of Regulatory And Mitochondrial Genetic Variants.” 2015. Doctoral Dissertation, Cornell University. Accessed March 08, 2021.
http://hdl.handle.net/1813/39371.
MLA Handbook (7th Edition):
Ye, Kaixiong. “The Evolutionary And Clinical Significance Of Regulatory And Mitochondrial Genetic Variants.” 2015. Web. 08 Mar 2021.
Vancouver:
Ye K. The Evolutionary And Clinical Significance Of Regulatory And Mitochondrial Genetic Variants. [Internet] [Doctoral dissertation]. Cornell University; 2015. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/1813/39371.
Council of Science Editors:
Ye K. The Evolutionary And Clinical Significance Of Regulatory And Mitochondrial Genetic Variants. [Doctoral Dissertation]. Cornell University; 2015. Available from: http://hdl.handle.net/1813/39371
Cornell University
16.
Chang, Hsinwen.
Transcriptional Network Regulated By Caenorhabditis Elegans Transcription Factors Ceh-23 And Cep-1, Modulates Lifespan Through Ampk Signalings When Mitochodnrial Electron Transport Chain.
Degree: PhD, Molecular and Cell Biology, 2015, Cornell University
URL: http://hdl.handle.net/1813/41092
► The global population is aging rapidly due to advances in technology and improvements in public health. Furthering knowledge about the aging process will allow discoveries…
(more)
▼ The global population is aging rapidly due to advances in technology and improvements in public health. Furthering knowledge about the aging process will allow discoveries of interventions and treatment to promote healthy aging that will hopefully, in turn, grant individuals access to a better quality of life during their later years. Several longevity modulators have been identified in various model organisms, and many of them seem to be conserved. One example of such a longevity modulator is the
mitochondrial electron transport chain (ETC) function.
Mitochondrial ETC function has long been associated with aging and lifespan determination, where moderately reduced
mitochondrial ETC function extends the lifespan of various organisms, suggesting that the pro-longevity effects of ETC function are well-conserved. The detailed mechanism of how
mitochondrial function affects organismal lifespan remains unknown. Several transcription factors have been shown to promote lifespan when
mitochondrial ETC function is impaired, suggesting that ETC dysfunction may induce a transcriptional network reprogramming response. Whether these transcription factors collaborate to modulate lifespan has not been fully explored. My thesis work shows that transcription factors CEH-23 and p53/CEP-1 likely collaborate to modulate lifespan under ETC stress as these transcription factors shows an epistatic relationship in their longevity effects. Consistently, microarray analyses revealed that CEH-23 and CEP-1 share a significant overlap in their transcriptional outputs, which are enriched in kinases and phosphatases. Intriguingly, the majority of CEH-23 and CEP-1 common targets are also regulated by AMP-activated protein kinase, suggesting that these two transcription factors engage AMPK signaling to modulate the lifespan of animals with impaired ETC. This study links the transcriptional response to the cell signaling response in organisms with impaired
mitochondrial ETC, which provides important insights into how mitochondria function to modulate organismal lifespan.
Advisors/Committee Members: Lee,Siu Sylvia (chair), Kemphues,Kenneth J (committee member), Fox,Thomas D. (committee member).
Subjects/Keywords: Aging; Mitochondrial function; Transcription
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APA (6th Edition):
Chang, H. (2015). Transcriptional Network Regulated By Caenorhabditis Elegans Transcription Factors Ceh-23 And Cep-1, Modulates Lifespan Through Ampk Signalings When Mitochodnrial Electron Transport Chain. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/41092
Chicago Manual of Style (16th Edition):
Chang, Hsinwen. “Transcriptional Network Regulated By Caenorhabditis Elegans Transcription Factors Ceh-23 And Cep-1, Modulates Lifespan Through Ampk Signalings When Mitochodnrial Electron Transport Chain.” 2015. Doctoral Dissertation, Cornell University. Accessed March 08, 2021.
http://hdl.handle.net/1813/41092.
MLA Handbook (7th Edition):
Chang, Hsinwen. “Transcriptional Network Regulated By Caenorhabditis Elegans Transcription Factors Ceh-23 And Cep-1, Modulates Lifespan Through Ampk Signalings When Mitochodnrial Electron Transport Chain.” 2015. Web. 08 Mar 2021.
Vancouver:
Chang H. Transcriptional Network Regulated By Caenorhabditis Elegans Transcription Factors Ceh-23 And Cep-1, Modulates Lifespan Through Ampk Signalings When Mitochodnrial Electron Transport Chain. [Internet] [Doctoral dissertation]. Cornell University; 2015. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/1813/41092.
Council of Science Editors:
Chang H. Transcriptional Network Regulated By Caenorhabditis Elegans Transcription Factors Ceh-23 And Cep-1, Modulates Lifespan Through Ampk Signalings When Mitochodnrial Electron Transport Chain. [Doctoral Dissertation]. Cornell University; 2015. Available from: http://hdl.handle.net/1813/41092
Victoria University of Wellington
17.
Hummel, Sonja.
Mitochondrial Transfer in Saccharomyces cerevisiae.
Degree: 2019, Victoria University of Wellington
URL: http://hdl.handle.net/10063/8123
► This thesis investigated mitochondrial transfer in Saccharomyces cerevisiae, between respiratory compromised B18p⁰ recipient and respiratory competent donor cells. The respiratory compromised strain had three red…
(more)
▼ This thesis investigated
mitochondrial transfer in Saccharomyces cerevisiae, between respiratory compromised B18p⁰ recipient and respiratory competent donor cells. The respiratory compromised strain had three red fluorescent proteins tagged to the membrane, nucleus and cytoplasm (triple RFP-B18p⁰) and is referred to as the B18p⁰ strain. B18p⁰ cells did not contain
mitochondrial DNA, causing it to be respiratory compromised and required a fermentable carbon source, such as glucose/dextrose, for proliferation. The respiratory competent strain used had a green fluorescent protein tagged to the Tom70
mitochondrial protein (Tom70-GFP) and is referred to as the Tom70 strain. The Tom70 cells contained the nuclear encoded URA3 cassette, allowing for negative selectivity of this strain using 5-FOA.
S. cerevisiae strains were co-cultured together in media containing only non-fermentable carbon sources (YPGE), plated on YPGE plates containing 5-FOA and colonies grown were distinguished post-co-culture based on their distinct phenotypic and genotypic characteristics. Fluorescent analysis of co-culture colonies revealed the presence of 5-FOA resistant Tom70 cells and some red B18p⁰ cells that had acquired the ability to grow on non-fermentable carbon sources. Genotypic analysis revealed that the majority of these red colonies had acquired mtDNA as well as the nuclear encoded, Tom70 specific URA3 cassette. Several permutations of co-cultures were performed, using different ratios of recipient and donor cells and single-gene deletion donor cells.
Purified mitochondria from Tom70 cells were tried to be transferred into B18p⁰ cells using centrifugation forces to induce a higher occurrence frequency of
mitochondrial transfer. Metabolic support experiments were conducted to investigate if the Tom70 strain could provide metabolic support to the B18p⁰ strain without
mitochondrial transfer.
Results indicate that no permutation induced potential
mitochondrial transfer at a higher rate than others. However, results indicate that
mitochondrial transfer did occur at low frequencies, potentially through the fusion of respiratory competent and respiratory compromised cells. Forced transfer did not increase the occurrence frequency of B18p⁰ cells to take up mitochondria and Tom70 cells did not provide metabolic support to B18p⁰ cells.
Advisors/Committee Members: McConnell, Melanie, Munkacsi, Andrew.
Subjects/Keywords: Mitochondrial transfer; Saccharomyces cerevisiae; Mitochondria
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Manager
APA (6th Edition):
Hummel, S. (2019). Mitochondrial Transfer in Saccharomyces cerevisiae. (Masters Thesis). Victoria University of Wellington. Retrieved from http://hdl.handle.net/10063/8123
Chicago Manual of Style (16th Edition):
Hummel, Sonja. “Mitochondrial Transfer in Saccharomyces cerevisiae.” 2019. Masters Thesis, Victoria University of Wellington. Accessed March 08, 2021.
http://hdl.handle.net/10063/8123.
MLA Handbook (7th Edition):
Hummel, Sonja. “Mitochondrial Transfer in Saccharomyces cerevisiae.” 2019. Web. 08 Mar 2021.
Vancouver:
Hummel S. Mitochondrial Transfer in Saccharomyces cerevisiae. [Internet] [Masters thesis]. Victoria University of Wellington; 2019. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/10063/8123.
Council of Science Editors:
Hummel S. Mitochondrial Transfer in Saccharomyces cerevisiae. [Masters Thesis]. Victoria University of Wellington; 2019. Available from: http://hdl.handle.net/10063/8123
University of Waikato
18.
Branford, Suzanne Nicola.
Grass carp and incidental invaders from aquaculture: a study of impacts on zooplankton communities and invader origins
.
Degree: 2016, University of Waikato
URL: http://hdl.handle.net/10289/10869
► The movement of fish from aquaculture facilities has led to invasions of non-native species globally, including of ‘hitch-hiking’ species, resulting in impacts on the composition…
(more)
▼ The movement of fish from aquaculture facilities has led to invasions of non-native species globally, including of ‘hitch-hiking’ species, resulting in impacts on the composition of communities in recipient ecosystems. This thesis employs both community scale analysis and sensitive molecular techniques to assess the effects of grass carp translocations on zooplankton communities and to determine the origins of an incidental non-native invader.
In the first component, I tested the effects of grass carp translocations from aquaculture facilities on ponds in the Auckland region, New Zealand. Zooplankton community composition was quantified in 34 ponds that had been
subject to grass carp release and 31 which had no grass carp introductions. A significant difference in zooplankton community composition was observed between ponds that had received grass carp translocations and those that had not. Differences in zooplankton community composition between ponds with and without carp releases were attributable to: 1) the establishment of zooplankton originating from aquaculture ponds, including non-native species; and 2) the effects of grass carp activity, through habitat modification. Effective measures to curb the proliferation of non-native taxa within aquaculture facilities, and to mitigate the unintentional movement of non-native taxa with translocations from these facilities, are required to reduce future introductions.
In the second component of this thesis I used a fragment of the
mitochondrial cytochrome c oxidase subunit I (COI) gene to more precisely identify the origins of invasions of freshwater calanoid copepod Skistodiaptomus pallidus (Herrick 1879). This was applied to populations sampled from within New Zealand, which have been linked to the release of fish from aquaculture facilities, and to populations found in Germany, which have possible links to a shipping vector. The S. pallidus COI sequences placed both the New Zealand and German specimens with those from the most easterly regions of the USA (e.g., New York, Virginia and Georgia). However, several haplotypes were found to be divergent between the New Zealand and German populations, indicating the exact sources of the introductions were likely different for each country. German sequences had greater haplotype diversity than those from New Zealand, supporting the suggestions of a shipping related vector of introduction to Germany. Both German and New Zealand populations contained haplotypes that were closely related to North American sequence records. However, further sampling of the native range will be required to determine the exact origin of the non-indigenous S. pallidus populations. With this additional information it may also be possible to determine more precisely the vectors of introduction.
Collectively, the two research chapters provide a broader understanding of invasion processes and the effects of grass carp translocations on the zooplankton communities within recipient ponds in New Zealand. My research has immediate application…
Advisors/Committee Members: Duggan, Ian C (advisor).
Subjects/Keywords: Biological Invasions;
Zooplankton;
Mitochondrial DNA
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APA ·
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APA (6th Edition):
Branford, S. N. (2016). Grass carp and incidental invaders from aquaculture: a study of impacts on zooplankton communities and invader origins
. (Masters Thesis). University of Waikato. Retrieved from http://hdl.handle.net/10289/10869
Chicago Manual of Style (16th Edition):
Branford, Suzanne Nicola. “Grass carp and incidental invaders from aquaculture: a study of impacts on zooplankton communities and invader origins
.” 2016. Masters Thesis, University of Waikato. Accessed March 08, 2021.
http://hdl.handle.net/10289/10869.
MLA Handbook (7th Edition):
Branford, Suzanne Nicola. “Grass carp and incidental invaders from aquaculture: a study of impacts on zooplankton communities and invader origins
.” 2016. Web. 08 Mar 2021.
Vancouver:
Branford SN. Grass carp and incidental invaders from aquaculture: a study of impacts on zooplankton communities and invader origins
. [Internet] [Masters thesis]. University of Waikato; 2016. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/10289/10869.
Council of Science Editors:
Branford SN. Grass carp and incidental invaders from aquaculture: a study of impacts on zooplankton communities and invader origins
. [Masters Thesis]. University of Waikato; 2016. Available from: http://hdl.handle.net/10289/10869
19.
이, 수진.
Protective effect of Nicotinamide on High glucose (HG)/Palmitate (PA)-induced Glucolipotoxicity to INS-1 beta cells.
Degree: 2013, Ajou University
URL: http://repository.ajou.ac.kr/handle/201003/8602
;
http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000014958
► Prolonged exposure of pancreatic beta cells to excessive levels of glucose and fatty acids is postulated to contribute to beta cell dysfunction and beta cell…
(more)
▼ Prolonged exposure of pancreatic beta cells to excessive levels of glucose and fatty acids is postulated to contribute to beta cell dysfunction and beta cell death in type 2 diabetes. Nicotinamide, via its major metabolite NAD+, is involved in a wide range of biological processes, including the production of energy. Nicotinamide (NAM) significantly protected the cells against the HG/PA-induced cell death. The aim of this study is to determine which mechanism of protective effect of nicotinamide on high glucose/palmitate (HG/PA)―induced INS-1 beta cell death. Protective effect of NAM was due to its role as an anti-oxidant, NAD+ precursor, or inhibitor of NAD+-consuming enzyme. first, Anti-oxidant activity of NAM was investigated whether other anti-oxidant have a protective effect on HG/PA-induced INS-1 cell death. Anti-oxidant such as NAD or GSH, or Mito-TEMPOL were not protective against HG/PA-induced cell death. Second, NAM had a restorative effect on NAD+ depletion was determined whether replenishment of NAD+ prevented HG/PA-induced cell death. Treatment with exogenous nicotinamide mononucleotide (NMN) or L-Kynurenin (Kyn), or nicotinamide adenine dinucleotide (NAD+) prevented HG/PA-induced viability reduction. but replenishment of NAD+ precursor did not have a protective effect against HG/PA-induced cell death. We have investigated whether NAD salvage pathway is involved in the protective effect of NAM on HG/PA-induced cell death. Inhibition of NAD salvage pathway by Nampt inhibitor FK866 or knocking down the Nampt or knocking down the Nmnat did not protect against HG/PA-induced cell death. Furthermore, FK866 did not reduced NAM-induced protective effects. Third, We have investigated whether NAM has protective effect against HG/PA-induced cell death through role of poly(ADP-ribose) polymerase (PARP), cADP-ribose synthase (CD38) or SIRT inhibitors in HG/PA-induced cell death. Pharmacologic inhibitors of PARP such as 3-AB and INH2BP or reduction of PARP using siRNA did not protect HG/PA-induced viability reduction and HG/PA-induced DNA fragmentation. Knock down or overexpression of CD38 did not protect HG/PA-induced viability reduction and HG/PA-induced Caspase3 induction. Resveratrol, SIRT activator, slightly augmented HG/PA-induced cell death. But Sirtinol, SIRT inhibitor slightly reduced HG/PA-induced cell death. Knockdown of Sirt3 or Sirt4 protected HG/PA-induced viability reduction and HG/PA-induced DNA fragmentation. In contrast, overexpression of Sirt3 or Sirt4 augmented HG/PA-induced cell death. NAM reduced the level of HG/PA-induced ER stress maker such as phospho-JNK, CHOP or calnexin, but increased the level of survival signal such as P-Akt. Collectively these data suggest that nicotinamide has protective effect through inhibition of mitochondrial Sirt3 and Sirt4 in HG/PA-induced INS-1 beta cell death.
높은 농도의 포도당과 지방산에 지속적으로 노출된 베타세포는 기능 이상에 이어 세포사멸이 유도되는데, 이는 제2형 당뇨병의 발병에 있어 중요한 병인이다. Nicotinamide (NAM)은 nicotinamide adenine dinucleotide (NAD+) 대사에 관련된 중요한 전구물질로 TCA 회로를 통한 에너지 생산에 관여하며 NAD+를 기질로 사용하는…
Advisors/Committee Members: 대학원 의생명과학과, 200924460, 이, 수진.
Subjects/Keywords: Glucolipotoxicity; Nicotinamide; NAD+; Mitochondrial Sirtuins
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APA (6th Edition):
이, . (2013). Protective effect of Nicotinamide on High glucose (HG)/Palmitate (PA)-induced Glucolipotoxicity to INS-1 beta cells. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/8602 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000014958
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
이, 수진. “Protective effect of Nicotinamide on High glucose (HG)/Palmitate (PA)-induced Glucolipotoxicity to INS-1 beta cells.” 2013. Thesis, Ajou University. Accessed March 08, 2021.
http://repository.ajou.ac.kr/handle/201003/8602 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000014958.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
이, 수진. “Protective effect of Nicotinamide on High glucose (HG)/Palmitate (PA)-induced Glucolipotoxicity to INS-1 beta cells.” 2013. Web. 08 Mar 2021.
Vancouver:
이 . Protective effect of Nicotinamide on High glucose (HG)/Palmitate (PA)-induced Glucolipotoxicity to INS-1 beta cells. [Internet] [Thesis]. Ajou University; 2013. [cited 2021 Mar 08].
Available from: http://repository.ajou.ac.kr/handle/201003/8602 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000014958.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
이 . Protective effect of Nicotinamide on High glucose (HG)/Palmitate (PA)-induced Glucolipotoxicity to INS-1 beta cells. [Thesis]. Ajou University; 2013. Available from: http://repository.ajou.ac.kr/handle/201003/8602 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000014958
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Miami
20.
Abrams, Alexander J.
Characterization of Novel Neurodegenerative Genes Implicated in Mitochondrial Dynamics.
Degree: PhD, Neuroscience (Medicine), 2016, University of Miami
URL: https://scholarlyrepository.miami.edu/oa_dissertations/1568
► Mitochondria are dynamic organelles undergoing constant fusion, fission, and migration within cells. The mobile nature of the mitochondria is essential for nerve health, as mutations…
(more)
▼ Mitochondria are dynamic organelles undergoing constant fusion, fission, and migration within cells. The mobile nature of the mitochondria is essential for nerve health, as mutations in two of the major
mitochondrial fusion genes, MFN21 and OPA12,3, cause axonal peripheral neuropathy (Charcot-Marie-Tooth Type 2, CMT2), and dominant optic atrophy (DOA) respectively. Through collaborative exome sequencing and data sharing, we identified four families with recessive mutations in the nuclear encoded
mitochondrial gene, SLC25A46 (Chapter 2). The patients in these families present a clinical spectrum of features ranging from optic atrophy, spasticity, peripheral neuropathy, and ataxia, to lethal infantile neurodegeneration. SLC25A46 is one of 53 members of the
mitochondrial solute carrier family (SLC25)11, which typically transport metabolites across the inner
mitochondrial membrane. Interestingly, SLC25A46 is similar to Ugo1, an essential component of the
mitochondrial fusion mechanism in yeast. However, unlike Ugo1, SLC25A46 seems to play a greater role in
mitochondrial fission in both cells and zebrafish models (Chapter 3). SLC25A46 strengthens the genetic overlap between optic atrophy and peripheral neuropathy, and is a novel
mitochondrial dynamic factor. While
mitochondrial dysfunctional plays a prominent role in nerve degeneration, abnormal protein aggregation is also another common feature. Here we describe a novel frame-shift mutation in NEFH associated with CMT2 in two families of dominant inheritance (Chapter 4). The frameshift mutations leads to the stop-loss and extended translation of 40 amino acids that would otherwise encode the 3’-UTR. Overexpression of this frameshift mutation in cultured cells results in prominent protein aggregation that is absent when wildtype NEFH is overexpressed. In vivo expression of the mutant protein in developing zebrafish larvae negatively affects the development of motor neurons in comparison to wildytpe NEFH overexpression. In conclusion, we have identified a novel
mitochondrial gene associated with dynamics, characterized a novel aggregation mechanism in neurofilaments, and developed models to study neurodegenerative diseases genes in zebrafish.
Advisors/Committee Members: Stephan Züchner, Julia Dallman, R. Grace Zhai, Juan Young, Mustafa Tekin.
Subjects/Keywords: Mitochondria; Mitochondrial Dynamics; Ugo1; SLC25A46
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APA (6th Edition):
Abrams, A. J. (2016). Characterization of Novel Neurodegenerative Genes Implicated in Mitochondrial Dynamics. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/1568
Chicago Manual of Style (16th Edition):
Abrams, Alexander J. “Characterization of Novel Neurodegenerative Genes Implicated in Mitochondrial Dynamics.” 2016. Doctoral Dissertation, University of Miami. Accessed March 08, 2021.
https://scholarlyrepository.miami.edu/oa_dissertations/1568.
MLA Handbook (7th Edition):
Abrams, Alexander J. “Characterization of Novel Neurodegenerative Genes Implicated in Mitochondrial Dynamics.” 2016. Web. 08 Mar 2021.
Vancouver:
Abrams AJ. Characterization of Novel Neurodegenerative Genes Implicated in Mitochondrial Dynamics. [Internet] [Doctoral dissertation]. University of Miami; 2016. [cited 2021 Mar 08].
Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1568.
Council of Science Editors:
Abrams AJ. Characterization of Novel Neurodegenerative Genes Implicated in Mitochondrial Dynamics. [Doctoral Dissertation]. University of Miami; 2016. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1568
University of Manitoba
21.
Mejia, Edgard Marcello.
Understanding the role of MLCL AT-1 and tafazzin in mitochondrial function.
Degree: Pharmacology and Therapeutics, 2015, University of Manitoba
URL: http://hdl.handle.net/1993/31584
► Cardiolipin (CL) is a phospholipid found exclusively in mitochondria and is required for normal mitochondrial function. CL biosynthesis requires a crucial remodelling step that incorporates…
(more)
▼ Cardiolipin (CL) is a phospholipid found exclusively in mitochondria and is required for normal
mitochondrial function. CL biosynthesis requires a crucial remodelling step that incorporates specific acyl chains onto its molecular structure. The enzyme primarily responsible for CL remodelling is Tafazzin (TAZ), a
mitochondrial protein encoded by the TAZ gene localized to chromosome Xq28.12. Mutations on the TAZ gene result in a rare yet severe disease known as Barth Syndrome (BTHS). BTHS is characterized by symptoms that include cardiomyopathies, neutropenia and skeletal myopathies. The
mitochondrial enzyme Monolysocardiolipin Acyltransferase -1 (MLCL AT-1) also exhibits the ability to remodel CL with specific acyl chains. The aims of our study were to 1) determine if a relationship exists between TAZ and MLCL AT-1 , 2) determine if MLCL AT-1 expression in BTHS lymphoblasts leads to improvements in
mitochondrial function, and 3) to use the Taz knockdown (KD) mouse model to get a better understanding of the phenotypes displayed by BTHS patients. Our results showed that in normal healthy lymphoblasts, expression of MLCL AT-1 was inversely dependent on TAZ expression. However, in BTHS lymphoblasts, expression of MLCL AT-1 was significantly lower compared to healthy controls. With the use of a MLCL AT-1-carrying plasmid, we expressed MLCL AT-1 in BTHS cells. This resulted in increased MLCL AT-1 gene, protein and enzyme activity. In addition, expression of MLCL AT-1 in BTHS cells resulted in increases in CL mass, improved
mitochondrial function and a reduction in reactive oxygen species (ROS) production. However, no changes were detected in
mitochondrial respiratory chain supercomplex (SC) assembly in BTHS cells expressing MLCL AT-1 compared to healthy controls. SC formation was disrupted in the hearts and skeletal muscle, but not the liver, of the Taz KD mice compared to wild-type (WT) animals. These results correlated with an elevated generation of hydrogen peroxide (H2O2) in the heart and skeletal muscle mitochondria of Taz KD mice compared to WT. Liver mitochondria from Taz KD mice, on the other hand, generated significantly less H2O2 compared to WT mice. The results from this study and our other published work demonstrate that MLCL AT-1 expression varies depending on the health of mitochondria and is tissue specific. In addition, our results reveal that TAZ expression is essential for various aspects of
mitochondrial function including SC formation and ROS production.
Advisors/Committee Members: Hatch, Grant (Pharmacology and Therapeutics) (supervisor), Hatch, Grant (Pharmacology and Therapeutics), Miller, Donald (Pharmacology and Therapeutics), Smyth, Donald (Pharmacology and Therapeutics), Triggs-Raine, Barbara (Biochemistry and Medical Genetics), McMaster, Christopher (Dalhousie University). (examiningcommittee).
Subjects/Keywords: Barth Syndrome; cardiolipin; mitochondrial function
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APA (6th Edition):
Mejia, E. M. (2015). Understanding the role of MLCL AT-1 and tafazzin in mitochondrial function. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/31584
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Mejia, Edgard Marcello. “Understanding the role of MLCL AT-1 and tafazzin in mitochondrial function.” 2015. Thesis, University of Manitoba. Accessed March 08, 2021.
http://hdl.handle.net/1993/31584.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Mejia, Edgard Marcello. “Understanding the role of MLCL AT-1 and tafazzin in mitochondrial function.” 2015. Web. 08 Mar 2021.
Vancouver:
Mejia EM. Understanding the role of MLCL AT-1 and tafazzin in mitochondrial function. [Internet] [Thesis]. University of Manitoba; 2015. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/1993/31584.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Mejia EM. Understanding the role of MLCL AT-1 and tafazzin in mitochondrial function. [Thesis]. University of Manitoba; 2015. Available from: http://hdl.handle.net/1993/31584
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Australian National University
22.
Gan, Lay Theng.
Mechanistic Studies of Cholesterol Lipotoxicity Pertinent to NASH
.
Degree: 2019, Australian National University
URL: http://hdl.handle.net/1885/182590
► Non-alcoholic fatty liver disease (NAFLD) affects ~30% of the world population with similar or higher prevalence in Australia. The pathology of NAFLD ranges from benign…
(more)
▼ Non-alcoholic fatty liver disease (NAFLD) affects ~30% of the
world population with similar or higher prevalence in Australia.
The pathology of NAFLD ranges from benign simple steatosis (SS)
to non-alcoholic steatohepatitis (NASH), with fibrosis that can
progress to cirrhosis. Understanding the pathogenesis of NASH
remains a challenge. In both humans and mice, obesity, diabetes
and metabolic syndrome are associated with NAFLD, but free
cholesterol (FC) accumulates in livers showing NASH but not in
those with SS. Such cholesterol-loaded livers are sensitised to
cytokine-mediated mitochondrial injury. However, at the time this
research was conducted, there was no direct evidence that linked
FC lipotoxicity to hepatocyte cell death or inflammatory
recruitment.
In this thesis, primary murine hepatocytes were loaded with FC by
exposing them to human low-density lipoprotein (LDL), and these
cells were used to characterise the mechanisms of hepatocellular
injury and cell death (apoptosis and necrosis). In particular we
tested the hypothesis that c-Jun N-terminal kinase (JNK)
activation and mitochondrial injury are essential steps in FC
hepatocellular lipotoxicity. We also examined how FC-injured
hepatocytes could promote activation of Kupffer cells (KC), which
is a key feature of liver inflammation in NASH.
The background to NAFLD and NASH as an important public health
problem, and as a liver disease is introduced in Chapter 1.
Concepts about NASH pathogenesis are discussed in light of
available knowledge up to the start of this PhD in 2011. The
common research materials and methods are discussed in Chapter
2.
In Chapter 3, the novel in vitro model of FC-loaded primary
murine hepatocytes is described. Briefly, primary murine
hepatocytes (C57B6/J wild type [WT]) were incubated with LDL
(0–40 µM), and shown to be loaded with FC. The subcellular
sites of primary hepatocyte FC were determined by co-localising
filipin fluorescence with organelle markers. The results were
compared with the intracellular distribution of FC seen in
atherogenic diet-fed foz/foz mouse livers, an in vivo model of
NASH. In mice with NASH, FC co-localised to plasma membrane (PM),
mitochondria and endoplasmic reticulum (ER) compartments. This
pattern was replicated in hepatocytes incubated with LDL to
dose-dependently increase hepatocyte FC. Further, FC loading
reduced PM fluidity and caused cell surface blebbing, with
release of extracellular vesicles (EVs), as evident on scanning
and transmission electron microscopy (EM).
In Chapter 4, the role of JNK1 in FC-mediated hepatocellular
injury was explored using primary hepatocytes from WT, Jnk1-/-and
Jnk2-/- mice. These cells were incubated with LDL (0–40 μM),
and molecular pathways of FC-mediated cell death determined by
western blot and…
Subjects/Keywords: cholesterol;
lipotoxicity;
NASH;
mitochondrial function
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Export
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APA (6th Edition):
Gan, L. T. (2019). Mechanistic Studies of Cholesterol Lipotoxicity Pertinent to NASH
. (Thesis). Australian National University. Retrieved from http://hdl.handle.net/1885/182590
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Gan, Lay Theng. “Mechanistic Studies of Cholesterol Lipotoxicity Pertinent to NASH
.” 2019. Thesis, Australian National University. Accessed March 08, 2021.
http://hdl.handle.net/1885/182590.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Gan, Lay Theng. “Mechanistic Studies of Cholesterol Lipotoxicity Pertinent to NASH
.” 2019. Web. 08 Mar 2021.
Vancouver:
Gan LT. Mechanistic Studies of Cholesterol Lipotoxicity Pertinent to NASH
. [Internet] [Thesis]. Australian National University; 2019. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/1885/182590.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Gan LT. Mechanistic Studies of Cholesterol Lipotoxicity Pertinent to NASH
. [Thesis]. Australian National University; 2019. Available from: http://hdl.handle.net/1885/182590
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Western Carolina University
23.
Stawski, Hilde.
Preparing whole genome human mitochondrial DNA libraries for
next generation sequencing using Illumina Nextera XT.
Degree: 2013, Western Carolina University
URL: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16380
► Forensic DNA casework principally relies on the analysis of short tandem repeats (STRs) from nuclear DNA (nDNA). In cases where nDNA may not be suitable…
(more)
▼ Forensic DNA casework principally relies on the
analysis of short tandem repeats (STRs) from nuclear DNA (nDNA). In
cases where nDNA may not be suitable for analysis (i.e., highly
degraded DNA or DNA present in quantities too low to obtain an STR
profile),
mitochondrial DNA (mtDNA) is an excellent alternative.
MtDNA is a circular genome of approximately 16.5 kb, is maternally
derived, and is present in thousands of copies per cell versus two
copies of nuclear DNA. The combined higher copy number, circular
shape of the genome and protection by the double membrane of the
mitochondrion allows for a greater probability to recover
sufficient mtDNA for typing of degraded samples. Presently,
forensic analysts sequence two or three hypervariable (HV) regions
found in the non-coding control region of the mtGenome, since
sequencing of the entire
mitochondrial genome (mtGenome) is rather
costly and labor-intensive. Additionally, difficulties sequencing
through homopolymeric regions, as well as the presence of lowlevel
mixtures in samples, can add complexity to the analysis of mtDNA in
casework when traditional Sanger sequencing methods are used. These
issues can be addressed with Next Generation Sequencing (NGS)
technologies. NGS enables deeper analysis of the genome for
identification of low-level mixtures, since clonal populations of
molecules originating from a single template strand are sequenced.
Moreover, this technology allows for the more cost-effective
sequencing of whole mtGenomes compared to Sanger methods, since
more sequences are obtained for the same sample. By expanding mtDNA
analysis to the entire mtGenome, a better resolution in
distinguishing between haplotypes is established. In forensic
casework, amplification of challenging samples such as hair and
aged bone is often performed differently than that of reference
samples (buccal swabs, blood, etc.) due to the higher possibility
of DNA degradation and limited mtDNA concentrations. For this
study, two sample preparation approaches were developed including
one method for robust reference samples, and one method for
forensically relevant challenging samples. For NGS analysis of
reference samples, DNA was extracted from buccal swabs obtained
from eight donors. A long PCR approach, which refers to the
amplification of DNA fragments of a size that may not be amplified
using conventional PCR reagents, was successfully performed on
these DNA extracts using a highly processive polymerase mixture and
novel primer pairs to amplify the mtGenome in two independent PCR
reactions, with overlap at the noncoding region. These samples were
subsequently processed with Illumina® Nextera® XT. This NGS library
preparation kit is designed exclusively for use with Illumina®
instrumentation and employs an engineered Transposome™ to randomly
fragment and tag amplicons and small genomes with Illumina®
specific adapters. After library preparation, samples were
sequenced on the Illumina® MiSeq™. This method generated whole
mtGenome NGS data, which accurately reflected the Sanger…
Advisors/Committee Members: Mark Wilson (advisor).
Subjects/Keywords: Mitochondrial DNA – Analysis – Data processing
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Stawski, H. (2013). Preparing whole genome human mitochondrial DNA libraries for
next generation sequencing using Illumina Nextera XT. (Masters Thesis). Western Carolina University. Retrieved from http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16380
Chicago Manual of Style (16th Edition):
Stawski, Hilde. “Preparing whole genome human mitochondrial DNA libraries for
next generation sequencing using Illumina Nextera XT.” 2013. Masters Thesis, Western Carolina University. Accessed March 08, 2021.
http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16380.
MLA Handbook (7th Edition):
Stawski, Hilde. “Preparing whole genome human mitochondrial DNA libraries for
next generation sequencing using Illumina Nextera XT.” 2013. Web. 08 Mar 2021.
Vancouver:
Stawski H. Preparing whole genome human mitochondrial DNA libraries for
next generation sequencing using Illumina Nextera XT. [Internet] [Masters thesis]. Western Carolina University; 2013. [cited 2021 Mar 08].
Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16380.
Council of Science Editors:
Stawski H. Preparing whole genome human mitochondrial DNA libraries for
next generation sequencing using Illumina Nextera XT. [Masters Thesis]. Western Carolina University; 2013. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16380
University of Melbourne
24.
Jackson, Christopher James.
Highly modified mitochondrial genomes: the case of the dinoflagellates.
Degree: 2011, University of Melbourne
URL: http://hdl.handle.net/11343/36514
► The mitochondrion is an indispensable organelle present in all eukaryotes, and is vital for energy metabolism as well as being implicated in iron homeostasis, fatty…
(more)
▼ The mitochondrion is an indispensable organelle present in all eukaryotes, and is vital for energy metabolism as well as being implicated in iron homeostasis, fatty acid and lipid biosynthesis. All mitochondria are derived from one endosymbiotic event, involving uptake of an α-proteobacterium, and with the exception of a few groups of anaerobic eukaryotes all mitochondria retain vestiges of their original bacterial genome. In comparison to the genomes of free-living bacteria, which are generally > 1 Mb and encode several thousand genes, mitochondrial genomes (mtDNAs) are highly reduced in both size and gene content. Moreover, some mtDNAs have evolved elaborate genome structures, sometimes involving multiple chromosomes, as well as complex gene organisations and gene expression processes. Hence, they have deviated significantly from the original endosymbiont bacterial genome.
Dinoflagellates are a large group of flagellated protists, and include both heterotrophic and autotrophic members. The closest relatives of the dinoflagellates are the apicomplexans, which are all obligate intracellular parasites, and the ciliates, a common protist group that is basal to the dinoflagellate and apicomplexan sister group. Together, the dinoflagellates, ciliates and apicomplexans form the group Alveolata. The mitochondrial genome of ciliates is relatively ‘normal’ in comparison to the majority of known mtDNAs, comprising a single linear chromosome ~40-50 kb in length, and encoding ~30 common mtDNA genes. Conversely, the apicomplexan genome (best known from the parasite Plasmodium, which causes malaria), is one of the most reduced mtDNAs known, comprising a tiny 6 kb chromosome that occurs as tandem repeats, and it encodes only three protein-coding genes (cox1, cox3 and cob) and two highly fragmented ribosomal RNAs (rRNAs). The alveolates therefore provide an excellent opportunity to investigate the evolution of highly divergent mitochondrial genomes. However, prior to this PhD little was known about the dinoflagellate mitochondrial genome. To compare the mtDNA states between dinoflagellates and other alveolates, and also within dinoflagellates, I have investigated the mtDNA gene content and gene organisation of two dinoflagellate species, Karlodinium micrum (synonyms: Karlodinium venificum, Ballantine) and Hematodinium sp. Hematodinium sp. is a basal dinoflagellate, whereas K. micrum branches higher within the majority of dinoflagellate diversity.
I have shown that the dinoflagellate mtDNA is one of the most complex known. My data strongly supports that, like in apicomplexans, the dinoflagellate mtDNA contains only cox1, cox3 and cob as well as two highly fragmented rRNAs. Unlike the apicomplexan mtDNA, all genes occur as multiple copies that occur in many genomic contexts. There is considerable predicted secondary structure present in intergenic regions. Further, in addition to full-length copies (with the exception of cox3 in K. micrum, which…
Subjects/Keywords: dinoflagellate; mitochondrial genome; organelle
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APA ·
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Export
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APA (6th Edition):
Jackson, C. J. (2011). Highly modified mitochondrial genomes: the case of the dinoflagellates. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/36514
Chicago Manual of Style (16th Edition):
Jackson, Christopher James. “Highly modified mitochondrial genomes: the case of the dinoflagellates.” 2011. Doctoral Dissertation, University of Melbourne. Accessed March 08, 2021.
http://hdl.handle.net/11343/36514.
MLA Handbook (7th Edition):
Jackson, Christopher James. “Highly modified mitochondrial genomes: the case of the dinoflagellates.” 2011. Web. 08 Mar 2021.
Vancouver:
Jackson CJ. Highly modified mitochondrial genomes: the case of the dinoflagellates. [Internet] [Doctoral dissertation]. University of Melbourne; 2011. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/11343/36514.
Council of Science Editors:
Jackson CJ. Highly modified mitochondrial genomes: the case of the dinoflagellates. [Doctoral Dissertation]. University of Melbourne; 2011. Available from: http://hdl.handle.net/11343/36514
Virginia Tech
25.
Flack, Kyle.
Effects of Resistance Training on aged Skeletal Muscle and Mitochondrial Function.
Degree: PhD, Human Nutrition, Foods, and Exercise, 2014, Virginia Tech
URL: http://hdl.handle.net/10919/25143
► With the aging of the baby boom population and an increased life expectancy, individuals aged 65 years and older are the fastest growing segment of…
(more)
▼ With the aging of the baby boom population and an increased life expectancy, individuals aged 65 years and older are the fastest growing segment of our population. Aging brings about changes in skeletal muscle such as reduced muscle strength and mass, as well as cellular deficits such as increased production of reactive oxygen species (ROS), and
mitochondrial DNA (MtDNA) deletions and mutations. Muscle mass declines at a rate of 1-2% each year after the age of 50, leading to muscle weakness, functional impairments, loss of independence, and an increase in falls. Additional declines in muscle mass and reduced muscle strength may result in a lower resting metabolic rate, reduced lipid oxidative capacity, increased adiposity, and insulin resistance. The rising number of individuals aged 65+ will increase demands on health care and health care costs, possibly leading to inadequate public resources and less care for the aged. This large societal impact, coupled with the aging of our population, suggests a clear need for methods that will improve the aging phenotype to enhance functionality, quality of life, and overall health for our aging population. This investigation aspires to delve into a relatively unexplored area of aging research and evaluate potential means that could help improve the aging phenotype.
The associated
mitochondrial impairments,
mitochondrial mediated apoptosis, and
mitochondrial DNA (MtDNA) deletions and mutations that accompany aging lead to a decline in physical fitness and oxidative capacity, and exercise has been shown to reverse or help prevent many of these disturbances. Resistance exercise training (RT) is currently the most effective known strategy to stimulate skeletal muscle hypertrophy and increase strength. Strength gains after RT lead to an improvement in activities of daily living and quality of life. There is some evidence suggesting that RT may lead to increased antioxidant enzyme capacity, decreased ROS production and increased electron transport chain (ETC) function in older individuals. The present study will lay a foundation for future research and further developments in the area of RT,
mitochondrial function and aging.
Advisors/Committee Members: Davy, Brenda M. (committeechair), Winett, Richard A. (committee member), Frisard, Madlyn I. (committee member), Hulver, Matthew W. (committee member), Davy, Kevin P. (committee member).
Subjects/Keywords: Resistance Training; Mitochondrial Function; Aging
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APA ·
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MLA ·
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Flack, K. (2014). Effects of Resistance Training on aged Skeletal Muscle and Mitochondrial Function. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/25143
Chicago Manual of Style (16th Edition):
Flack, Kyle. “Effects of Resistance Training on aged Skeletal Muscle and Mitochondrial Function.” 2014. Doctoral Dissertation, Virginia Tech. Accessed March 08, 2021.
http://hdl.handle.net/10919/25143.
MLA Handbook (7th Edition):
Flack, Kyle. “Effects of Resistance Training on aged Skeletal Muscle and Mitochondrial Function.” 2014. Web. 08 Mar 2021.
Vancouver:
Flack K. Effects of Resistance Training on aged Skeletal Muscle and Mitochondrial Function. [Internet] [Doctoral dissertation]. Virginia Tech; 2014. [cited 2021 Mar 08].
Available from: http://hdl.handle.net/10919/25143.
Council of Science Editors:
Flack K. Effects of Resistance Training on aged Skeletal Muscle and Mitochondrial Function. [Doctoral Dissertation]. Virginia Tech; 2014. Available from: http://hdl.handle.net/10919/25143
Michigan State University
26.
So, Minyoung.
Structure and physiology of mitochondrial replicative DNA helicases.
Degree: 2017, Michigan State University
URL: http://etd.lib.msu.edu/islandora/object/etd:4659
► Thesis Ph. D. Michigan State University. Biochemistry and Molecular Biology 2017
The mitochondrial replicative DNA helicase (mtDNA helicase) unwinds double-stranded mitochondrial DNA (mtDNA) by using…
(more)
▼ Thesis Ph. D. Michigan State University. Biochemistry and Molecular Biology 2017
The mitochondrial replicative DNA helicase (mtDNA helicase) unwinds double-stranded mitochondrial DNA (mtDNA) by using NTP hydrolysis at the mtDNA replication fork. Moreover, single-stranded DNA annealing activity and branch migration are identified in human mtDNA helicase, expanding its roles in mtDNA repair or recombination. The mtDNA helicase is also proposed to tether mitochondrial nucleoid to the mitochondrial inner membrane or to load itself on the closed DNA. Consequently, defects in the mtDNA helicase gene cause several mitochondrial diseases. I have pursued a comprehensive understanding of the structural and functional roles for both human and Drosophila mtDNA helicases and Drosophila Ind1, a putative interacting partner of the Drosophila mtDNA helicase, in mitochondrial DNA maintenance. In particular, research in this dissertation has focused mainly on the N-terminal primase-like domains, which have no primase activity in metazoan mtDNA helicases and contain a species-specific iron-sulfur cluster in Drosophila mtDNA helicase. Structural studies of human mtDNA helicase present several different oligomeric states and structural dynamicity of its full-length form and demonstrate that the zinc binding-like domain imparts the structural flexibility to the helicase. In addition, open-ring structures and one-arm extended structures are observed, supporting a self-loading mechanism (Chapter 2). Functional studies in chapter 3 suggest that the N-terminal domains of the mtDNA helicases function as a binding module that interacts with a metal cofactor, lipid, and single-stranded DNA. I confirm the presence of the iron-sulfur cluster in the N-terminal domain of Drosophila mtDNA helicase and also show that the N-terminal domain serves a role in membrane binding through electrostatic interactions with cardiolipin. In addition, the positively-charged region where pathogenic mutants are clustered in the RNA polymerase-like domain of human mtDNA helicase contributes to single-stranded DNA binding that is likely required to mtDNA helicase self-loading, translocation, and annealing (Chapter 3). Drosophila Ind1, as a putative iron-sulfur donor to Drosophila mtDNA helicase, has been characterized. Its mitochondrial localization, dimerization, and the membrane binding property driven by electrostatic and hydrophobic interactions were demonstrated. In particular, the membrane binding property of Drosophila Ind1 may facilitate the transfer of an iron-sulfur cluster to membrane-bound recipients: complex I and possibly Drosophila mtDNA helicase (Chapter 4). Although the putative interaction between the mtDNA helicase and the Ind1 was not detected under given conditions in this research, I hypothesize that the expected protein-protein interactions may occur under optimized conditions with an appropriate cofactor (ATP) and chaperone proteins, based on experimental results and comparison with other protein in its Mrp/ MinD family in chapter 4. Including…
Advisors/Committee Members: Kaguni, Laurie S., Henry, Bill R., LaPres, John J., Kuo, Min-Hao, Gallo, Kathleen A..
Subjects/Keywords: DNA helicases; Mitochondrial DNA; Biochemistry
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APA ·
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Export
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Manager
APA (6th Edition):
So, M. (2017). Structure and physiology of mitochondrial replicative DNA helicases. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:4659
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
So, Minyoung. “Structure and physiology of mitochondrial replicative DNA helicases.” 2017. Thesis, Michigan State University. Accessed March 08, 2021.
http://etd.lib.msu.edu/islandora/object/etd:4659.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
So, Minyoung. “Structure and physiology of mitochondrial replicative DNA helicases.” 2017. Web. 08 Mar 2021.
Vancouver:
So M. Structure and physiology of mitochondrial replicative DNA helicases. [Internet] [Thesis]. Michigan State University; 2017. [cited 2021 Mar 08].
Available from: http://etd.lib.msu.edu/islandora/object/etd:4659.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
So M. Structure and physiology of mitochondrial replicative DNA helicases. [Thesis]. Michigan State University; 2017. Available from: http://etd.lib.msu.edu/islandora/object/etd:4659
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Michigan State University
27.
Farnum, Gregory Alan.
Experimental and theoretical studies of the mitochondrial replisome.
Degree: 2013, Michigan State University
URL: http://etd.lib.msu.edu/islandora/object/etd:2966
► Thesis M.S. Michigan State University. Biochemistry and Molecular Biology 2013.
Despite the ubiquitous trend of increasing complexity in eukaryotes, the vital process of mtDNA replication…
(more)
▼ Thesis M.S. Michigan State University. Biochemistry and Molecular Biology 2013.
Despite the ubiquitous trend of increasing complexity in eukaryotes, the vital process of mtDNA replication has retained a simplistic, three component replisome consisting of the mtDNA Pol γ, mtSSB and the mtDNA replicative helicase. This minimal mitochondrial replisome resembles the bacteriophage T7 replisome and may even be simpler due to the apparent absence of a primase function in the N-terminal domain of the mtDNA replicative helicase. Interestingly, insects have retained the four cysteines of motif I which have been shown to bind zinc in T7, so an N-terminal construct (NTD) of Drosophila melanogaster mtDNA replicative helicase was designed containing the conserved residues. Purified fractions of the NTD construct contain an iron sulfur cluster, as determined by UV-Visible spectroscopy, as well as iron and sulfide determination. This work describes for the first time an iron sulfur cluster site in dm-mtDNA replicative helicase and evidence of weak DNA binding by the NTD using a FRET assay. Mutations in Pol γ represent a major cause of human mitochondrial diseases, especially those affecting the nervous system in adults and in children. More than 160 POLG1 disease mutations have been identified, which are nearly uniformly distributed along the length of the POLG1 sequence. Comprehensive literature analysis of the biochemical properties and disease characteristics of Pol γ in light of the crystal structure have revealed genotype-phenotype correlations that support the clustering of mutations into five functional modules in the catalytic core of Pol γ. Our results suggest that cluster prediction can be used to evaluate both the likely biochemical defects and the relative pathogenicity of new POLG variants.
Description based on online resource; title from PDF t.p. (viewed on Sept. 18, 2014)
Advisors/Committee Members: Kaguni, Laurie A, Geiger, James, Ferguson-Miller, Shelagh M.
Subjects/Keywords: Mitochondrial DNA; DNA replication; Biochemistry
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Export
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APA (6th Edition):
Farnum, G. A. (2013). Experimental and theoretical studies of the mitochondrial replisome. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:2966
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Farnum, Gregory Alan. “Experimental and theoretical studies of the mitochondrial replisome.” 2013. Thesis, Michigan State University. Accessed March 08, 2021.
http://etd.lib.msu.edu/islandora/object/etd:2966.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Farnum, Gregory Alan. “Experimental and theoretical studies of the mitochondrial replisome.” 2013. Web. 08 Mar 2021.
Vancouver:
Farnum GA. Experimental and theoretical studies of the mitochondrial replisome. [Internet] [Thesis]. Michigan State University; 2013. [cited 2021 Mar 08].
Available from: http://etd.lib.msu.edu/islandora/object/etd:2966.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Farnum GA. Experimental and theoretical studies of the mitochondrial replisome. [Thesis]. Michigan State University; 2013. Available from: http://etd.lib.msu.edu/islandora/object/etd:2966
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
28.
NC DOCKS at Western Carolina University; Stawski, Hilde.
Preparing whole genome human mitochondrial DNA libraries for next generation sequencing using Illumina Nextera XT.
Degree: 2013, NC Docks
URL: http://libres.uncg.edu/ir/wcu/f/Stawski2013.pdf
► Forensic DNA casework principally relies on the analysis of short tandem repeats (STRs) from nuclear DNA (nDNA). In cases where nDNA may not be suitable…
(more)
▼ Forensic DNA casework principally relies on the analysis of short tandem repeats
(STRs) from nuclear DNA (nDNA). In cases where nDNA may not be suitable for
analysis (i.e., highly degraded DNA or DNA present in quantities too low to obtain an
STR profile), mitochondrial DNA (mtDNA) is an excellent alternative. MtDNA is a
circular genome of approximately 16.5 kb, is maternally derived, and is present in
thousands of copies per cell versus two copies of nuclear DNA. The combined higher
copy number, circular shape of the genome and protection by the double membrane of
the mitochondrion allows for a greater probability to recover sufficient mtDNA for typing
of degraded samples.
Presently, forensic analysts sequence two or three hypervariable (HV) regions
found in the non-coding control region of the mtGenome, since sequencing of the entire
mitochondrial genome (mtGenome) is rather costly and labor-intensive. Additionally,
difficulties sequencing through homopolymeric regions, as well as the presence of lowlevel
mixtures in samples, can add complexity to the analysis of mtDNA in casework
when traditional Sanger sequencing methods are used. These issues can be addressed with Next Generation Sequencing (NGS) technologies. NGS enables deeper analysis of
the genome for identification of low-level mixtures, since clonal populations of
molecules originating from a single template strand are sequenced. Moreover, this
technology allows for the more cost-effective sequencing of whole mtGenomes compared
to Sanger methods, since more sequences are obtained for the same sample. By
expanding mtDNA analysis to the entire mtGenome, a better resolution in distinguishing
between haplotypes is established.
In forensic casework, amplification of challenging samples such as hair and aged
bone is often performed differently than that of reference samples (buccal swabs, blood,
etc.) due to the higher possibility of DNA degradation and limited mtDNA
concentrations. For this study, two sample preparation approaches were developed
including one method for robust reference samples, and one method for forensically
relevant challenging samples.
For NGS analysis of reference samples, DNA was extracted from buccal swabs
obtained from eight donors. A long PCR approach, which refers to the amplification of
DNA fragments of a size that may not be amplified using conventional PCR reagents,
was successfully performed on these DNA extracts using a highly processive polymerase
mixture and novel primer pairs to amplify the mtGenome in two independent PCR
reactions, with overlap at the noncoding region. These samples were subsequently
processed with Illumina® Nextera® XT. This NGS library preparation kit is designed
exclusively for use with Illumina® instrumentation and employs an engineered Transposome™ to randomly fragment and tag amplicons and small genomes with
Illumina® specific adapters. After library preparation, samples were sequenced on the
Illumina® MiSeq™. This method generated whole mtGenome NGS data, which
accurately reflected the Sanger…
Subjects/Keywords: Mitochondrial DNA – Analysis – Data processing
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APA (6th Edition):
NC DOCKS at Western Carolina University; Stawski, H. (2013). Preparing whole genome human mitochondrial DNA libraries for next generation sequencing using Illumina Nextera XT. (Thesis). NC Docks. Retrieved from http://libres.uncg.edu/ir/wcu/f/Stawski2013.pdf
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
NC DOCKS at Western Carolina University; Stawski, Hilde. “Preparing whole genome human mitochondrial DNA libraries for next generation sequencing using Illumina Nextera XT.” 2013. Thesis, NC Docks. Accessed March 08, 2021.
http://libres.uncg.edu/ir/wcu/f/Stawski2013.pdf.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
NC DOCKS at Western Carolina University; Stawski, Hilde. “Preparing whole genome human mitochondrial DNA libraries for next generation sequencing using Illumina Nextera XT.” 2013. Web. 08 Mar 2021.
Vancouver:
NC DOCKS at Western Carolina University; Stawski H. Preparing whole genome human mitochondrial DNA libraries for next generation sequencing using Illumina Nextera XT. [Internet] [Thesis]. NC Docks; 2013. [cited 2021 Mar 08].
Available from: http://libres.uncg.edu/ir/wcu/f/Stawski2013.pdf.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
NC DOCKS at Western Carolina University; Stawski H. Preparing whole genome human mitochondrial DNA libraries for next generation sequencing using Illumina Nextera XT. [Thesis]. NC Docks; 2013. Available from: http://libres.uncg.edu/ir/wcu/f/Stawski2013.pdf
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of California – Irvine
29.
Fiss, Ashlynn Nicole.
An Assessment of the Mitochondrial Disease Community’s Knowledge and Perception of the “Three-Person Baby,” or MRT, and the Impact of the Media Debate that Surrounds this Technique.
Degree: Genetic Counseling, 2016, University of California – Irvine
URL: http://www.escholarship.org/uc/item/75r0w31g
► This study was designed to assess the mitochondrial disease community’s knowledge, attitude and perception of mitochondrial replacement therapy (MRT) and determine how the media can…
(more)
▼ This study was designed to assess the mitochondrial disease community’s knowledge, attitude and perception of mitochondrial replacement therapy (MRT) and determine how the media can impact such perception. MRT in conjunction with in vitro fertilization (IVF) has the ability to prevent inheritance of mitochondrial DNA (mtDNA) mutations from mothers to their offspring by using a donor egg’s mtDNA. The Federal Drug Administration (FDA) is considering human trials for MRT, dubbed “three-parent IVF” by the media. Approval relies heavily on the mitochondrial disease community’s willingness to participate; however, the community’s perceptions of risks, benefits and limitations associated with MRT have not been adequately addressed. An anonymous survey was distributed online to individuals within the mitochondrial community; 165 individuals completed the survey and comprised the study population. The majority of individuals found MRT ethical, agreed with FDA approval for human clinical trials, and would be willing to use MRT if clinically appropriate and available. However, almost half were unaware that MRT is only useful if a mtDNA mutation has been previously identified. Many respondents knew this technique does not change physical or personality traits of offspring; however, those who believed it did also felt more strongly that this technique is “designing babies”. Interestingly, the majority did not believe that the children born using MRT have three parents, so the media’s use of “three-parent baby” may be unnecessarily sensationalized. Our results provide evidence that the mitochondrial disease community is forward-thinking about MRT; however, may not be adequately aware of MRT’s risks or limitations.
Subjects/Keywords: Genetics; Assisted reproductive technology; Mitochondrial disease; Mitochondrial Replacement Therapy
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APA ·
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APA (6th Edition):
Fiss, A. N. (2016). An Assessment of the Mitochondrial Disease Community’s Knowledge and Perception of the “Three-Person Baby,” or MRT, and the Impact of the Media Debate that Surrounds this Technique. (Thesis). University of California – Irvine. Retrieved from http://www.escholarship.org/uc/item/75r0w31g
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Fiss, Ashlynn Nicole. “An Assessment of the Mitochondrial Disease Community’s Knowledge and Perception of the “Three-Person Baby,” or MRT, and the Impact of the Media Debate that Surrounds this Technique.” 2016. Thesis, University of California – Irvine. Accessed March 08, 2021.
http://www.escholarship.org/uc/item/75r0w31g.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Fiss, Ashlynn Nicole. “An Assessment of the Mitochondrial Disease Community’s Knowledge and Perception of the “Three-Person Baby,” or MRT, and the Impact of the Media Debate that Surrounds this Technique.” 2016. Web. 08 Mar 2021.
Vancouver:
Fiss AN. An Assessment of the Mitochondrial Disease Community’s Knowledge and Perception of the “Three-Person Baby,” or MRT, and the Impact of the Media Debate that Surrounds this Technique. [Internet] [Thesis]. University of California – Irvine; 2016. [cited 2021 Mar 08].
Available from: http://www.escholarship.org/uc/item/75r0w31g.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Fiss AN. An Assessment of the Mitochondrial Disease Community’s Knowledge and Perception of the “Three-Person Baby,” or MRT, and the Impact of the Media Debate that Surrounds this Technique. [Thesis]. University of California – Irvine; 2016. Available from: http://www.escholarship.org/uc/item/75r0w31g
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of California – Irvine
30.
Simon, Mariella T.
Mitochondrial Metabolism and Morphology in Mitochondrial Disease States.
Degree: Biological Sciences, 2016, University of California – Irvine
URL: http://www.escholarship.org/uc/item/7ss5250z
► ABSTRACT OF THE DISSERTATIONMitochondrial Metabolism and Morphologyin Mitochondrial Disease StatesByMariella Theresa SimonDoctor of Philosophy in Biological SciencesUniversity of California, Irvine, 2016Professor Susanne Rafelski, ChairMitochondria are…
(more)
▼ ABSTRACT OF THE DISSERTATIONMitochondrial Metabolism and Morphologyin Mitochondrial Disease StatesByMariella Theresa SimonDoctor of Philosophy in Biological SciencesUniversity of California, Irvine, 2016Professor Susanne Rafelski, ChairMitochondria are the hub of cellular metabolism, respiration and energy production. They are sites of reactive oxidative species (ROS), heme and steroid generation. They buffer cellular calcium flux, regulate redox states, control cell cycle and death and are therefore at the nexus of human health and disease. Syndromes encountered in the mitochondrial disease clinic, associated with mutations in mitochondrial genes, are generally rare and require detailed clinical mitochondrial disease workups, including next generation sequencing technology. The discovery of new genes often presents itself with inconclusive findings, which need to be further pursued and delineated in the research setting. It is therefore of great importance to apply the “bedside to bench and back to bedside” principle in the field of mitochondrial medicine to advance diagnostic and treatment modalities. In this dissertation, I demonstrate bioenergetic findings in three novel mitochondrial disease genes, NARS2, TFAM and LonP1, in a collaborative effort. By doing so, I have helped to delineate the underlying cause of pathologies for families with mitochondrial disease. Presented are also two case studies of patients with mutations in POLG and GFM1, with unusual clinical findings, which may point to new, not yet described cellular processes associated with mitochondrial dysfunction. By correlating gene function with patient’s disease, taking into consideration clinical parameters observed, I have also shown new metabolic findings in a primary fibroblast tissue culture system from patients with mutations in the mitochondrial matrix protease LonP1. The patients have mutations in a domain of the gene, which has never been associated with disease. Findings suggest that the patient phenotype depends on the location of the mutations in LonP1 and that clinical expression is domain specific. Findings also show increased susceptibility to stress, elicited by the use of antibiotic/antimycotic in the tissue culture system. In the future, I plan to build on the results from this study, to assess the effects of potential treatment modalities on mitochondrial function in fibroblast culture.
Subjects/Keywords: Cellular biology; Genetics; Leigh Syndrome; LonP1; Mitochondrial Disease; Mitochondrial Myopathy; Nars2
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Record Details
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❌
APA ·
Chicago ·
MLA ·
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Manager
APA (6th Edition):
Simon, M. T. (2016). Mitochondrial Metabolism and Morphology in Mitochondrial Disease States. (Thesis). University of California – Irvine. Retrieved from http://www.escholarship.org/uc/item/7ss5250z
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Simon, Mariella T. “Mitochondrial Metabolism and Morphology in Mitochondrial Disease States.” 2016. Thesis, University of California – Irvine. Accessed March 08, 2021.
http://www.escholarship.org/uc/item/7ss5250z.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Simon, Mariella T. “Mitochondrial Metabolism and Morphology in Mitochondrial Disease States.” 2016. Web. 08 Mar 2021.
Vancouver:
Simon MT. Mitochondrial Metabolism and Morphology in Mitochondrial Disease States. [Internet] [Thesis]. University of California – Irvine; 2016. [cited 2021 Mar 08].
Available from: http://www.escholarship.org/uc/item/7ss5250z.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Simon MT. Mitochondrial Metabolism and Morphology in Mitochondrial Disease States. [Thesis]. University of California – Irvine; 2016. Available from: http://www.escholarship.org/uc/item/7ss5250z
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
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Open Access Theses and Dissertations