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Rutgers University
1.
Bai, Zhiyong, 1982-.
A study of retrograde transport using Caenorhabditis elegans intestinal cells as a model.
Degree: PhD, Cell and Developmental Biology, 2015, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/48386/ 
► Endocytosis mediates the internalization of cell surface proteins and lipids in small vesicles that bud from the plasma membrane and deliver their cargo to endosomes.…
(more)
▼ Endocytosis mediates the internalization of cell surface proteins and lipids in small vesicles that bud from the plasma membrane and deliver their cargo to endosomes. When cargo proteins reach the endosomes, one important pathway that they may follow is retrograde transport, in which cargos are delivered from endosomes to the Golgi apparatus. The role of the recycling endosome in retrograde transport has not been studied well in the past. We use C. elegans, especially the intestinal cells, as model to study retrograde trafficking, employing a combination of genetics, cell biology, biochemistry and molecular biology tools. We discovered that CDC-42/TOCAs/PARs/WAVE localize to the recycling endosome, and regulate retrograde transport at a step from Recycling endosome to Trans-Golgi Network. When missing functional CDC-42/TOCAs/PARs/WAVE, MIG-14/Wntless is misdirected to the late endosome/lysosome during post-endocytic sorting, and steady-state MIG-14 protein levels are strongly reduced. Neuronal polarity defects in mechanosensory neurons ALM are also observed under these conditions, consistent with a defect in MIG-14-dependent WNT signaling. Interestingly, we also found that mutants lacking retromer components SNX-3, VPS-35, VPS-26, or VPS-29, that aberrantly degrade MIG-14 during retrograde transport, also aberrantly degrade the human Transferrin receptor during early endosome to recycling endosome transport. Furthermore, we tested TGN-38, the worm homolog of a well known retrograde cargo TGN38 that passes through the recycling endosome. When missing functional CDC-42, TGN-38 is mainly trapped at the recycling endosome, while upon loss of functional SNX-3, TGN-38 is trapped at the early endosome. These results suggest CDC-42/TOCAs/PARs/WAVE regulate retrograde transport at a step from Recycling endosome to the Trans-Golgi Network after SNX-3/VPS-35/VPS-26/VPS-29, which regulates early endosome to recycling endosome transport. Lastly, we obtained evidence that CDC-42/TOCAs/PARs/WAVE complex may use clathrin/AP-1 vesicles, and that OCRL-1/CKII may work with CDC-42/TOCAs/PARs/WAVE and regulate retrograde transport from the recycling endosome to Trans-Golgi Network. We hope that our work will shed light on the study of intracellular trafficking, especially retrograde transport.
Advisors/Committee Members: Barr, Maureen (chair), Grant, Barth (co-chair), Rongo, Christopher (internal member), Kramer, Sunita (outside member).
Subjects/Keywords: Caenorhabditis elegans
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APA (6th Edition):
Bai, Zhiyong, 1. (2015). A study of retrograde transport using Caenorhabditis elegans intestinal cells as a model. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/48386/
Chicago Manual of Style (16th Edition):
Bai, Zhiyong, 1982-. “A study of retrograde transport using Caenorhabditis elegans intestinal cells as a model.” 2015. Doctoral Dissertation, Rutgers University. Accessed March 07, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/48386/.
MLA Handbook (7th Edition):
Bai, Zhiyong, 1982-. “A study of retrograde transport using Caenorhabditis elegans intestinal cells as a model.” 2015. Web. 07 Mar 2021.
Vancouver:
Bai, Zhiyong 1. A study of retrograde transport using Caenorhabditis elegans intestinal cells as a model. [Internet] [Doctoral dissertation]. Rutgers University; 2015. [cited 2021 Mar 07].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/48386/.
Council of Science Editors:
Bai, Zhiyong 1. A study of retrograde transport using Caenorhabditis elegans intestinal cells as a model. [Doctoral Dissertation]. Rutgers University; 2015. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/48386/
Columbia University
2.
Deng, Yuting.
Novel negative regulation of LIN-12/Notch in Caenorhabditis elegans.
Degree: 2016, Columbia University
URL: https://doi.org/10.7916/D8KS6RVT
► Proper cell fate specification is crucial for development, and dysregulation in cellular signaling pathways can lead to deleterious effects like cancer. The conserved LIN- 12/Notch…
(more)
▼ Proper cell fate specification is crucial for development, and dysregulation in cellular signaling pathways can lead to deleterious effects like cancer. The conserved LIN- 12/Notch signaling pathway mediates fate specification in many cellular contexts, and multiple regulatory mechanisms ensures appropriate LIN-12/Notch activity in each context. Here, I have identified several cis-regulatory domains and trans-acting factors that contribute to the negative regulation of LIN-12/Notch in Caenorhabditis elegans.
In this thesis, I find that LIN-12/Notch requires binding to LAG-1/CSL and association with the nuclear complex for protein turnover in the C. elegans vulval precursor cells (VPCs). I also identify two layers of negative regulation in the VPCs and their descendants. The E3 ubiquitin ligase SEL-10/Fbw7 mediates degradation of LIN-12/Notch via the PEST domain in the VPCs, while a novel structural conformation in the C-terminal end of the LIN-12/Notch intracellular domain is required for downregulation in the descendants.
Through an RNAi screen for negative regulators, I isolated 13 conserved kinases that downregulate LIN-12/Notch activity. Of these 13 kinases, CDK-8 had been previously implicated in Notch turnover, while the other 12 are novel negative regulators. I provide evidence that 5 of the kinases regulate LIN-12/Notch through modulation of the intracellular domain. Furthermore, I conduct a deeper investigation into CDK-8, which is the kinase component of the Mediator complex. I determine that CDK-8 acts with the rest of the Cdk8 Kinase Module and independent of the Mediator core to negatively regulate LIN-12/Notch, and that CDK-8 kinase activity is required for this process. Lastly, I find that sur-2/MED23 and lin-25/MED24 are required for LIN-12/Notch ligand transcription, independent of the Cdk8 Kinase Module and Mediator Head and Tail components.
Subjects/Keywords: Caenorhabditis elegans – Genetics; Genetics; Caenorhabditis elegans
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APA (6th Edition):
Deng, Y. (2016). Novel negative regulation of LIN-12/Notch in Caenorhabditis elegans. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8KS6RVT
Chicago Manual of Style (16th Edition):
Deng, Yuting. “Novel negative regulation of LIN-12/Notch in Caenorhabditis elegans.” 2016. Doctoral Dissertation, Columbia University. Accessed March 07, 2021.
https://doi.org/10.7916/D8KS6RVT.
MLA Handbook (7th Edition):
Deng, Yuting. “Novel negative regulation of LIN-12/Notch in Caenorhabditis elegans.” 2016. Web. 07 Mar 2021.
Vancouver:
Deng Y. Novel negative regulation of LIN-12/Notch in Caenorhabditis elegans. [Internet] [Doctoral dissertation]. Columbia University; 2016. [cited 2021 Mar 07].
Available from: https://doi.org/10.7916/D8KS6RVT.
Council of Science Editors:
Deng Y. Novel negative regulation of LIN-12/Notch in Caenorhabditis elegans. [Doctoral Dissertation]. Columbia University; 2016. Available from: https://doi.org/10.7916/D8KS6RVT
Oregon State University
3.
Wernick, Riana I.
Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans.
Degree: PhD, Zoology, 2016, Oregon State University
URL: http://hdl.handle.net/1957/59186
► Understanding the impact of mitochondrial dysfunction on genome evolution has the potential not only to provide new insights on the basic evolutionary processes influencing mitochondrial…
(more)
▼ Understanding the impact of mitochondrial dysfunction on genome evolution has the potential not only to provide new insights on the basic evolutionary processes influencing mitochondrial and nuclear genomes, but may also reveal novel avenues for evolutionary adaptive recovery from harmful mutations. Aberrant mitochondrial activity is fundamental to the pathology of mitochondrial diseases in addition to neurodegenerative disorders. While the effects of mitochondrial dysfunction have received much attention, less is known about their impact on genome evolution and potential target mechanisms for ameliorating the harmful effects of mitochondrial impairment. Characterizing genome modifications in animal populations predisposed to mitochondrial dysfunction may identify novel genes, mechanisms, and physiological pathways to target for recovery and provides a genome-wide perspective on the impact of aberrant mitochondrial activity.
This dissertation research investigates how mitochondrial and nuclear genomes evolve in organisms genetically predisposed to mitochondrial dysfunction and contrasts genomic evolution in large and small population sizes. This work furthers understanding of the impact of evolutionary forces which influence genome evolution in population with reduced fitness, and reveals new insights into genomic responses to mitochondrial dysfunction. Chapters 2 and 3 of this dissertation focus on genome evolution using a set of mitochondrial respiratory chain mutant (gas-1¬ strain) and wild-type (N2 strain)
Caenorhabditis elegans mutation-accumulation (MA) lines that experienced single-worm bottlenecking. The N2 MA lines, derived from a previous experiment, were bottlenecked for 250 generations. The gas-1 MA lines were created for this research, and bottlenecked in the laboratory for a maximum of 50 generations. Chapter 2 investigates mitogenomic evolution and heteroplasmic inheritance patterns evolving under extreme drift in gas-1 and N2 MA lines. Chapter 3 analyzes nuclear genome evolution using this same set of gas-1 and N2 MA lines. In contrast, Chapter 4 provides a complementary perspective, analyzing mitochondrial and nuclear genome evolution in twenty-four gas-1 'recovery line' (RC) populations, evolved in large population sizes for sixty generations. Bioinformatic methods and computational simulations were applied to characterize and evaluate genome evolution and provide a comprehensive investigation of the impact of mitochondrial dysfunction within a population genetics framework.
In Chapter 2 our results of inherited mitochondrial DNA (mtDNA) heteroplasmy are in alignment with predictions of theories where a small subset of mtDNA molecules from the parental generation repopulates the mitochondrial genome pool for the progeny. Comparisons between Chapter 2 and 4 suggest that in both gas-1 and N2 strains organelle genome copy number is elevated in an environment characterized with extreme genetic drift but is less impacted throughout evolution in large populations when the force of genetic drift is…
Advisors/Committee Members: Denver, Dee R. (advisor), Perez, Viviana (committee member).
Subjects/Keywords: Mitochondria; Caenorhabditis elegans
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APA (6th Edition):
Wernick, R. I. (2016). Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/59186
Chicago Manual of Style (16th Edition):
Wernick, Riana I. “Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans.” 2016. Doctoral Dissertation, Oregon State University. Accessed March 07, 2021.
http://hdl.handle.net/1957/59186.
MLA Handbook (7th Edition):
Wernick, Riana I. “Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans.” 2016. Web. 07 Mar 2021.
Vancouver:
Wernick RI. Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans. [Internet] [Doctoral dissertation]. Oregon State University; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1957/59186.
Council of Science Editors:
Wernick RI. Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans. [Doctoral Dissertation]. Oregon State University; 2016. Available from: http://hdl.handle.net/1957/59186
Universidad de Valladolid
4.
García Casas, Paloma.
Calcium signaling modulators: a novel pharmacological intervention to delay aging in Caenorhabditis elegans.
Degree: 2020, Universidad de Valladolid
URL: http://uvadoc.uva.es/handle/10324/43492
► Ca2+ is a second messenger that affects nearly every aspect or cellular life including muscle contraction, neuronal secretion and cell proliferation and differentiation. The dysregulation…
(more)
▼ Ca2+ is a second messenger that affects nearly every aspect or cellular life
including muscle contraction, neuronal secretion and cell proliferation and
differentiation. The dysregulation of the cellular toolkit that controls and
maintains Ca2+ homeostasis has been linked to the physiopathology of the aging
process including neurodegeneration. Caenorhabditis elegans has been proven to
be an excellent model organism to study aging and neurodegeneration due to the
conservation of numerous signaling pathways that have been proven to modulate
aging, and the availability of several models of neurodegenerative diseases.
Moreover, the interrelationship between aging and Ca2+ signaling can be studied
in the worms because of their transparent cuticle that allows to perform in vivo
Ca2+ dynamics studies throughout the whole life of the organisms.
The metabolic pathways that are known to regulate aging in C. elegans are
the so called nutrient sensing pathways. All these pathways, that are conserved in
mammals, are able to respond to changes in nutrient availability that, in the end,
affect the longevity of the worms. These pathways are the insulin/insulin-likegrowth
factor (IGF-1) signaling pathway (IIS), the mechanistic target of rapamycin
(mTOR) signaling pathway, the adenosine monophosphate-activated protein
kinase (AMPK) pathway, and the sirtuins pathway. Although not much
information about how intracellular Ca2+ regulates these pathways, there is some
evidence that suggests that Ca2+ might be implicated in the modulation of nutrient
sensing pathways activities.
This thesis has focused in the study of the interrelationship between Ca2+
signaling and nutrient sensing pathways, and its possible effects in the aging
process through two different pharmacological approaches: the submaximal
inhibition of sarco-endoplasmic reticulum calcium-ATPase (SERCA) using 2,5-BHQ
and thapsigargin, and the submaximal inhibition of the mitochondrial Na+/Ca2+
exchanger using CGP37157.
SERCA refills the endoplasmic reticulum (ER) with Ca2+ up to the millimolar
range being the main controller of the ER [Ca2+] level, implicated in the modulation
of cytosolic Ca2+ signaling and ER-mitochondria Ca2+ transfer. In this work it has
been proven that the submaximal inhibition of SERCA with 2,5-BHQ and
thapsigargin induced an increase in the lifespan of C. elegans worms and that this
effect was mediated by the modulation of mTOR and AMPK signaling pathways.
Moreover, it was also discarded that the effect was mediated by the activation of
the ER stress response.
CGP37157 is a benzothiazepine with neuroprotective effects in several in vitro
models of excitotoxicity involving dysregulation of intracellular Ca2+ homeostasis.
CGP37157 has been used for decades as an inhibitor of the mitochondrial Na+/Ca2+
20 exchanger (mNCX), although several off targets have been described. Throughout
this thesis, the effects of CGP37157 in C. elegans healthspan, as well as its possible
modulation of nutrient sensing pathways and Ca2+…
Subjects/Keywords: Calcio; Caenorhabditis elegans
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APA ·
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APA (6th Edition):
García Casas, P. (2020). Calcium signaling modulators: a novel pharmacological intervention to delay aging in Caenorhabditis elegans. (Thesis). Universidad de Valladolid. Retrieved from http://uvadoc.uva.es/handle/10324/43492
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):
García Casas, Paloma. “Calcium signaling modulators: a novel pharmacological intervention to delay aging in Caenorhabditis elegans.” 2020. Thesis, Universidad de Valladolid. Accessed March 07, 2021.
http://uvadoc.uva.es/handle/10324/43492.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
García Casas, Paloma. “Calcium signaling modulators: a novel pharmacological intervention to delay aging in Caenorhabditis elegans.” 2020. Web. 07 Mar 2021.
Vancouver:
García Casas P. Calcium signaling modulators: a novel pharmacological intervention to delay aging in Caenorhabditis elegans. [Internet] [Thesis]. Universidad de Valladolid; 2020. [cited 2021 Mar 07].
Available from: http://uvadoc.uva.es/handle/10324/43492.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
García Casas P. Calcium signaling modulators: a novel pharmacological intervention to delay aging in Caenorhabditis elegans. [Thesis]. Universidad de Valladolid; 2020. Available from: http://uvadoc.uva.es/handle/10324/43492
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Rutgers University
5.
Gleason, Adenrele Madeline, 1982-.
Endocytic recycling in Caenorhabditis elegans.
Degree: PhD, Cell and Developmental Biology, 2016, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/51295/
► The power of conservation is exemplified in the C. elegans intestinal epithelia. As a model to study endocytic recycling, molecular transport regulators have been characterized…
(more)
▼ The power of conservation is exemplified in the C. elegans intestinal epithelia. As a model to study endocytic recycling, molecular transport regulators have been characterized in this genetically tractable system. In this dissertation, I describe the molecular requirements for Syndpin/SDPN-1 in vivo. Proteoliposome assays confirm that full-length SDPN-1 is capable of tubulating acidic liposomes in vitro. As a likely accessory protein, SDPN-1 coordinates the exit of recycling cargo from the early endosome. I propose that Syndapin/SDPN-1 facilitates this transport step through the localized recruitment of actin to early endosomes. In addition, the worm intestine provides a lucid understanding of the endosomal determinates that coordinate TGFβ signaling. We report TGFβ signaling and internalization require Clathrin-Dependent Endocytosis (CDE). Furthermore, post internalization of the receptors result in the sorting of the type I and the type II receptors into distinct molecular sorting complexes. Mutants defective in retromer-dependent recycling missort their type I SMA-6 to the lysosome and impair signaling. Alternatively, the type II receptor, DAF-4 (dauer formation defective-4) is returned through the ARF-6 (ADP-ribosylation factor-6) dependent recycling pathway.
Advisors/Committee Members: Grant, Barth D (chair).
Subjects/Keywords: Caenorhabditis elegans; Endocytosis
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APA (6th Edition):
Gleason, Adenrele Madeline, 1. (2016). Endocytic recycling in Caenorhabditis elegans. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/51295/
Chicago Manual of Style (16th Edition):
Gleason, Adenrele Madeline, 1982-. “Endocytic recycling in Caenorhabditis elegans.” 2016. Doctoral Dissertation, Rutgers University. Accessed March 07, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/51295/.
MLA Handbook (7th Edition):
Gleason, Adenrele Madeline, 1982-. “Endocytic recycling in Caenorhabditis elegans.” 2016. Web. 07 Mar 2021.
Vancouver:
Gleason, Adenrele Madeline 1. Endocytic recycling in Caenorhabditis elegans. [Internet] [Doctoral dissertation]. Rutgers University; 2016. [cited 2021 Mar 07].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/51295/.
Council of Science Editors:
Gleason, Adenrele Madeline 1. Endocytic recycling in Caenorhabditis elegans. [Doctoral Dissertation]. Rutgers University; 2016. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/51295/
Rutgers University
6.
Raduwan, Hamidah, 1988-.
The RhoGAPs RGA-8/RICH-1/SH3BP1 and HUM-7/Myo9 regulate actomyosin enrichment during C. elegans embryonic morphogenesis.
Degree: PhD, Cell and Developmental Biology, 2019, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/60048/
► Organ and tissue formation are highly regulated processes during embryonic development. Defects in this process can lead to birth defects, or premature death. The complexity…
(more)
▼ Organ and tissue formation are highly regulated processes during embryonic development. Defects in this process can lead to birth defects, or premature death. The complexity of vertebrate tissues complicates the study of organ and tissue embryonic development. Epidermal morphogenesis in the nematode Caenorhabditis elegans is an ideal model to study tissue morphogenesis in whole organisms. C. elegans is amenable to genetics and microscopy observation, allowing us to capture live imaging of the migrating tissues. Previous studies from our lab identified a Rac1-dependent branched actin pathway as an important regulator of epidermal cell migration during this process. However, the role of actomyosin contractility during this process was unclear. Actin dynamics and actomyosin contractility are regulated by the Rho GTPases protein family. Rac1 and Cdc42 promote branched actin formation, while Cdc42 and RhoA promote actomyosin contractility. Rho GTPases are molecular switches that become activated by binding to GTP, and deactivated by hydrolyzing GTP to become GDP. The cycle of GTP- and GDP- binding is regulated by GTP exchange factor proteins (GEFs) and GTPase-activating proteins (GAPs), respectively. C. elegans only has seven members of Rho GTPases, but 23 GAPs, suggesting layers of regulation in
ii
the process of branched actin formation and actomyosin contractility. In this study we performed the first characterization of two RhoGAPs, RGA-8/RICH-1/SH3BP1 and HUM-7/Myo9 and show that they regulate morphogenesis in C. elegans by modulating RHO-1/RhoA and CDC-42. We show that RGA-8/RICH-1/SH3BP1 and HUM-7/Myo9 regulate myosin enrichment during morphogenesis, including at the epidermal pocket cells during ventral enclosure. Previous studies proposed actomyosin contractility is mainly required in underlying neuroblasts to promote epidermal cell migrations. In contrast, the results here show that myosin is polarized, and tightly regulated in the migrating epidermal cells, by RGA-8/RICH- 1/SH3BP1 and HUM-7/Myo9. In addition, we show these proteins contribute to normal morphogenesis by regulating the timing of morphogenetic cell movements. Overall, we place the RhoGAPs HUM-7/Myo9 and RGA-8/RICH-1/SH3BP1 in pathways that regulate both actin and actomyosin contractility through RHO-1 and CDC-42, demonstrating new roles for these GTPases in embryonic epidermal morphogenesis in C. elegans.
Advisors/Committee Members: Irvine, Kenneth (chair), Soto, Martha (internal member), Wadsworth, William (internal member), Bennett, Joan (outside member), School of Graduate Studies.
Subjects/Keywords: Caenorhabditis elegans; Morphogenesis
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APA ·
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APA (6th Edition):
Raduwan, Hamidah, 1. (2019). The RhoGAPs RGA-8/RICH-1/SH3BP1 and HUM-7/Myo9 regulate actomyosin enrichment during C. elegans embryonic morphogenesis. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/60048/
Chicago Manual of Style (16th Edition):
Raduwan, Hamidah, 1988-. “The RhoGAPs RGA-8/RICH-1/SH3BP1 and HUM-7/Myo9 regulate actomyosin enrichment during C. elegans embryonic morphogenesis.” 2019. Doctoral Dissertation, Rutgers University. Accessed March 07, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/60048/.
MLA Handbook (7th Edition):
Raduwan, Hamidah, 1988-. “The RhoGAPs RGA-8/RICH-1/SH3BP1 and HUM-7/Myo9 regulate actomyosin enrichment during C. elegans embryonic morphogenesis.” 2019. Web. 07 Mar 2021.
Vancouver:
Raduwan, Hamidah 1. The RhoGAPs RGA-8/RICH-1/SH3BP1 and HUM-7/Myo9 regulate actomyosin enrichment during C. elegans embryonic morphogenesis. [Internet] [Doctoral dissertation]. Rutgers University; 2019. [cited 2021 Mar 07].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60048/.
Council of Science Editors:
Raduwan, Hamidah 1. The RhoGAPs RGA-8/RICH-1/SH3BP1 and HUM-7/Myo9 regulate actomyosin enrichment during C. elegans embryonic morphogenesis. [Doctoral Dissertation]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60048/
Rutgers University
7.
Smolyn, Jennifer, 1992-.
The first characterization of the WASH complex in C. elegans endocytic recycling.
Degree: MS, Cell and Developmental Biology, 2020, Rutgers University
URL: https://rucore.libraries.rutgers.edu/rutgers-lib/62566/
► The quantity and distribution of proteins in the plasma membrane play an essential role in regulating a cell’s response to its environment and resulting physiology.…
(more)
▼ The quantity and distribution of proteins in the plasma membrane play an essential role in regulating a cell’s response to its environment and resulting physiology. This cell surface protein mosaic is largely influenced by the endocytic recycling pathway, misregulation of which has been implicated in a variety of human conditions, including neurodegenerative diseases and cancer. Endocytosis and subsequent intracellular movement of cargo requires both membrane fission and vesicle movement, with the force for these processes provided by a spatially and temporally regulated dynamic branched actin network, generated by Arp2/3-mediated actin polymerization. While it has been determined that endocytosis requires the nucleation promoting factors WASP and WAVE at the plasma membrane, a role for the structurally-related WASH complex for this process in C.
elegans remains more elusive. In mammalian systems, the WASH complex seems to act at early endosomes, facilitating retrograde trafficking via its FAM21 subunit interacting with retromer. However, a homologous protein to FAM21 in the
Caenorhabditis elegans WASH complex has yet to be identified. This work provides the first characterization of the C.
elegans WASH complex, detailing its function on RAB-5-, PI(3)P-positive early endosomes to ensure proper sorting during endocytic recycling, likely through retrograde trafficking to the Golgi apparatus. Through RNAis and genetic crosses, these experiments reveal a functionally important role for the WASH complex in this pathway that is distinct from other nucleation promoting factors, including the WAVE complex, despite similarities between the two. Furthermore, proper recycling may be mediated in part by the protein C05G5.2, as these data suggest this could be the previously unidentified C.
elegans FAM21 homolog.
Advisors/Committee Members: Soto, Martha (chair), Grant, Barth (co-chair), Wadsworth, William (co-chair), School of Graduate Studies.
Subjects/Keywords: WASH; Caenorhabditis elegans
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APA (6th Edition):
Smolyn, Jennifer, 1. (2020). The first characterization of the WASH complex in C. elegans endocytic recycling. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/62566/
Chicago Manual of Style (16th Edition):
Smolyn, Jennifer, 1992-. “The first characterization of the WASH complex in C. elegans endocytic recycling.” 2020. Masters Thesis, Rutgers University. Accessed March 07, 2021.
https://rucore.libraries.rutgers.edu/rutgers-lib/62566/.
MLA Handbook (7th Edition):
Smolyn, Jennifer, 1992-. “The first characterization of the WASH complex in C. elegans endocytic recycling.” 2020. Web. 07 Mar 2021.
Vancouver:
Smolyn, Jennifer 1. The first characterization of the WASH complex in C. elegans endocytic recycling. [Internet] [Masters thesis]. Rutgers University; 2020. [cited 2021 Mar 07].
Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/62566/.
Council of Science Editors:
Smolyn, Jennifer 1. The first characterization of the WASH complex in C. elegans endocytic recycling. [Masters Thesis]. Rutgers University; 2020. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/62566/
University of Utah
8.
Welker, Noah Christopher.
The Role of Caenorhabditis Elegans Dicer in Endogenous Small RNA Silencing Pathways.
Degree: PhD, Biochemistry;, 2010, University of Utah
URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/715/rec/1217
► RNA interference (RNAi) was originally identified as a conserved biological response to exogenous double-stranded RNA (dsRNA). During this response, dsRNA is processed into 21-23 nucleotide…
(more)
▼ RNA interference (RNAi) was originally identified as a conserved biological response to exogenous double-stranded RNA (dsRNA). During this response, dsRNA is processed into 21-23 nucleotide small interfering RNAs (siRNAs) by the ribonuclease III enzyme Dicer. siRNAs produced by this pathway initiate the sequence specific degradation of their cognate messenger RNAs (mRNAs). While RNAi was originally discovered as a response to exogenous dsRNA, during the time of my dissertation research, it has become clear that endogenous dsRNA is responsible for regulating many biological processes. Dicer is also responsible for processing endogenous dsRNA in the form of micro- RNAs (miRNAs) and many endogenous-siRNAs (endo-siRNAs). The effects that Dicer dependent endo-siRNAs and miRNAs have on their cognate mRNAs was unclear prior to the work described in this dissertation. In Chapter 2, I describe my work to characterize how transcripts are misregulated in C. elegans harboring a mutation in the dcr-1 gene. I found that Dicer is responsible for regulating a large number of transcripts including known and predicted miRNA targets. Among the misregulated transcripts in dcr-1 (-/-) was an enrichment for genes involved in C. elegans innate immunity. This later finding prompted me to investigate the role of Dicer's helicase domain, particularly in light of this domain's similarity to RIG-I and MDA-5, two mammalian helicases involved in innate immunity. In Chapter 3,1 describe experiments in which I reintroduced the dcr-1 gene with targeted mutations in the helicase domain into dcr-1 (-/-) C. elegans. Reintroduction of either wild-type (WT) or helicase mutant dcr-1 rescued the fertility defects exhibited in dcr-1 (-/-) animals. Furthermore, I show that dcr-1 helicase mutants have a normal RNAi response following feeding of exogenous dsRNA. I present deep sequencing data that indicates that while dcr-1 helicase mutants process miRNAs to WT levels, they are defective for the production some, but not all, endo-siRNAs. In light of these data, I present a model for Dicer cleavage in which Dicer acts as a processive translocase to process long dsRNA to siRNAs. In Chapter 4, I propose experiments to test this model in light of current literature.
Subjects/Keywords: Small Interfering RNA; Caenorhabditis elegans
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APA (6th Edition):
Welker, N. C. (2010). The Role of Caenorhabditis Elegans Dicer in Endogenous Small RNA Silencing Pathways. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/715/rec/1217
Chicago Manual of Style (16th Edition):
Welker, Noah Christopher. “The Role of Caenorhabditis Elegans Dicer in Endogenous Small RNA Silencing Pathways.” 2010. Doctoral Dissertation, University of Utah. Accessed March 07, 2021.
http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/715/rec/1217.
MLA Handbook (7th Edition):
Welker, Noah Christopher. “The Role of Caenorhabditis Elegans Dicer in Endogenous Small RNA Silencing Pathways.” 2010. Web. 07 Mar 2021.
Vancouver:
Welker NC. The Role of Caenorhabditis Elegans Dicer in Endogenous Small RNA Silencing Pathways. [Internet] [Doctoral dissertation]. University of Utah; 2010. [cited 2021 Mar 07].
Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/715/rec/1217.
Council of Science Editors:
Welker NC. The Role of Caenorhabditis Elegans Dicer in Endogenous Small RNA Silencing Pathways. [Doctoral Dissertation]. University of Utah; 2010. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/715/rec/1217
9.
村田, 大輔.
A study on biological roles of GPI-anchor synthesis in the germline development of the nematode Caenorhabditis elegans : 線虫Caenorhabditis elegansの生殖系列細胞発生におけるGPIアンカー合成の生物学的役割に関する研究.
Degree: 博士（理学）, 2013, Kyushu University / 九州大学
URL: http://hdl.handle.net/2324/21716
;
http://dx.doi.org/10.15017/21716
► Glycosylphosphatidylinositol (GPI)-anchor attachment is one of the most common posttranslational protein modifications. Using the nematode Caenorhabditis elegans, we determined that GPI-anchored proteins are present in…
(more)
▼ Glycosylphosphatidylinositol (GPI)-anchor attachment is one of the most common posttranslational protein modifications. Using the nematode
Caenorhabditis elegans, we determined that GPI-anchored proteins are present in germline cells and distal tip cells, which are essential for the maintenance of the germline stem cell niche. We identified 24 C.
elegans genes involved in GPI-anchor synthesis. Inhibition of various steps of GPI-anchor synthesis by RNA interference or gene knockout resulted in abnormal development of oocytes and early embryos, and both lethal and sterile phenotypes were observed. The piga-1 gene (orthologue of human PIGA) codes for the catalytic subunit of the phosphatidylinositol N-acetylglucosaminyltransferase complex, which catalyzes the first step of GPI-anchor synthesis. We isolated piga-1–knockout worms and found that GPI-anchor synthesis is indispensable for the maintenance of mitotic germline cell number. The knockout worms displayed 100% lethality, with decreased mitotic germline cells and abnormal eggshell formation. Using cell-specific rescue of the null allele, we showed that expression of piga-1 in somatic gonads and/or in germline is sufficient for normal embryonic development and the maintenance of the germline mitotic cells. These results clearly demonstrate that GPI-anchor synthesis is indispensable for germline formation and for normal development of oocytes and eggs.
Advisors/Committee Members: 野村, 一也.
Subjects/Keywords: Caenorhabditis elegans; GPI-anchor
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APA (6th Edition):
村田, . (2013). A study on biological roles of GPI-anchor synthesis in the germline development of the nematode Caenorhabditis elegans : 線虫Caenorhabditis elegansの生殖系列細胞発生におけるGPIアンカー合成の生物学的役割に関する研究. (Thesis). Kyushu University / 九州大学. Retrieved from http://hdl.handle.net/2324/21716 ; http://dx.doi.org/10.15017/21716
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):
村田, 大輔. “A study on biological roles of GPI-anchor synthesis in the germline development of the nematode Caenorhabditis elegans : 線虫Caenorhabditis elegansの生殖系列細胞発生におけるGPIアンカー合成の生物学的役割に関する研究.” 2013. Thesis, Kyushu University / 九州大学. Accessed March 07, 2021.
http://hdl.handle.net/2324/21716 ; http://dx.doi.org/10.15017/21716.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
村田, 大輔. “A study on biological roles of GPI-anchor synthesis in the germline development of the nematode Caenorhabditis elegans : 線虫Caenorhabditis elegansの生殖系列細胞発生におけるGPIアンカー合成の生物学的役割に関する研究.” 2013. Web. 07 Mar 2021.
Vancouver:
村田 . A study on biological roles of GPI-anchor synthesis in the germline development of the nematode Caenorhabditis elegans : 線虫Caenorhabditis elegansの生殖系列細胞発生におけるGPIアンカー合成の生物学的役割に関する研究. [Internet] [Thesis]. Kyushu University / 九州大学; 2013. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2324/21716 ; http://dx.doi.org/10.15017/21716.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
村田 . A study on biological roles of GPI-anchor synthesis in the germline development of the nematode Caenorhabditis elegans : 線虫Caenorhabditis elegansの生殖系列細胞発生におけるGPIアンカー合成の生物学的役割に関する研究. [Thesis]. Kyushu University / 九州大学; 2013. Available from: http://hdl.handle.net/2324/21716 ; http://dx.doi.org/10.15017/21716
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Texas Southwestern Medical Center
10.
Song, Bo-mi.
Familiar Food-Induced Feeding Activation in C. Elegans.
Degree: 2011, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/887
► The growing epidemic of obesity and eating disorders demands the study of regulatory mechanisms of food intake. Studying mutants whose food intake is altered under…
(more)
▼ The growing epidemic of obesity and eating disorders demands the study of regulatory mechanisms of food intake. Studying mutants whose food intake is altered under various conditions has greatly advanced our understanding of the mechanism. However, it is still largely unknown by which mechanisms perception of food activates food intake. The simple anatomy, genetic tractability, and well-characterized and quantifiable feeding behavior and evolutionary conservation of feeding regulators make C.
elegans an attractive model system for the study. Food intake in C.
elegans requires two muscle motions, pharyngeal pumping and isthmus peristalsis, and the frequencies of the two feeding motions dramatically increase in response to food as in other organisms. I attempted to understand the mechanism underlying food-induced feeding activation by studying the mechanism and the physiological context of action of serotonin, an endogenous activator of pharyngeal pumping. Here I show that like food, serotonin increases overall feeding by activating both feeding motions. Serotonin activates the two feeding motions by activating two distinct neural pathways. A 5-HT7 receptor activated the two motions mainly by acting in the two distinct pharyngeal motor neurons that are essential for food-induced feeding activation. Moreover, the results support that the serotonin receptor activated the two distinct neurons mainly by activating two distinct downstream G protein signaling pathways. Despite the separate regulation, isthmus peristalsis was coupled to the preceding pharyngeal pump. The separate regulation with coupling of the two feeding motions may have evolved to support efficient feeding by allowing control of the ratio of the frequencies of the two muscle motions according to density of food and by preventing futile isthmus peristalsis. Then, which aspect of food triggers the serotonin signal that increases food intake? I found that recognition of familiar food selectively triggers the serotonin signal. Worms selectively consume particular bacteria more actively after experience and the behavioral plasticity requires serotonin signaling. By dissecting the mechanism, I found that recognition of familiar food triggers serotonin release from a pair of chemosensory neurons. The released serotonin acts as an endocrine signal to increase pharyngeal pumping rate by activating the pharyngeal motor neuron that directly triggers pharyngeal pumping. The results suggest that worms form a memory of previously experienced food and that the memory controls food intake. Consistently, the familiar-food induced feeding was strongly dependent on duration of exposure to food to learn but not developmental timing of exposure or nutritional status. Furthermore, worms could remember the previously experienced food at least for several hours. My study provides insight into how feeding organ operates to increase food intake in response to food and how a particular aspect of food controls the process to increase food intake in C.
elegans.…
Advisors/Committee Members: Avery, Leon.
Subjects/Keywords: Caenorhabditis elegans; Feeding Behavior; Serotonin
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APA ·
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CSE |
Export
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Manager
APA (6th Edition):
Song, B. (2011). Familiar Food-Induced Feeding Activation in C. Elegans. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/887
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, Bo-mi. “Familiar Food-Induced Feeding Activation in C. Elegans.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021.
http://hdl.handle.net/2152.5/887.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Song, Bo-mi. “Familiar Food-Induced Feeding Activation in C. Elegans.” 2011. Web. 07 Mar 2021.
Vancouver:
Song B. Familiar Food-Induced Feeding Activation in C. Elegans. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2152.5/887.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Song B. Familiar Food-Induced Feeding Activation in C. Elegans. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/887
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Manchester
11.
Vargas, Miguel.
Nutrient Response and Aging in Invertebrate
Models.
Degree: 2013, University of Manchester
URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:185790
► The diet an organism keeps is crucial in sustaining its health and fitness. The fruit fly Drosophila melanogaster and the nematode Caenorhabditis elegans are excellent…
(more)
▼ The diet an organism keeps is crucial in sustaining
its health and fitness. The fruit fly Drosophila melanogaster and
the nematode
Caenorhabditis elegans are excellent models for
nutritional studies due to their small size, large progeny numbers,
quick development, and modifiable laboratory diets. Here I examine
these two organisms in order to better understand the complex
interrelationship between an animal and its diet. Previous work has
shown that in the wild numerous organisms are capable of selecting
specific nutrients in a non-random manner in order to maximize
fitness. However, the genetic underpinnings driving these nutrient
choices remain elusive. Female fruit flies consume higher levels of
protein following mating to prepare for the costs of reproduction.
I examined the role of S6 Kinase (S6K), a downstream effector of
the nutrient-responsive target of rapamycin pathway, in mediating
this decision. I demonstrate that neuronal S6K activity and
serotonin are involved in regulating protein consumption when
allowed to choose nutrients freely as well as following
macronutrient deprivation; suggesting that they may play a role in
mediating postmating dietary switch and maintaining nutrient
balance. Modulating levels of dietary components can have extensive
impacts on processes such as development, fecundity, and metabolism
in multiple organisms. However, the influence of dietary genetics
on the consumer is virtually unknown. I performed a screen feeding
single-gene mutants of E. coli to C.
elegans and monitored the
effects on the insulin-like signalling pathway (ILS). When mutated,
genes involved in multiple processes and functions in E. coli
enhanced activity of the ILS downstream transcription factor,
DAF-16. One mutant strain of E. coli I pursued had a knockout of
the cAMP-producing, adenylate cyclase gene. Addition of exogenous
cAMP to the diet containing live, metabolically active E. coli
rescued all the effects of the mutant on C.
elegans; thereby
suggesting that bacterial metabolism of dietary cAMP can influence
the C.
elegans ILS. Collectively, my work demonstrates how the
nutrient-sensing pathways of the consumer can shape and be shaped
by interactions with its diet. These studies contribute to a better
understanding of the consumer-diet relationship, and could help
guide future work to investigate the role of diet in disease,
quality of life, and longevity.
Advisors/Committee Members: PAVITT, GRAHAM GD, Hubbard, Simon, Pavitt, Graham.
Subjects/Keywords: Drosophila Melanogaster; Caenorhabditis Elegans; Diet
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APA ·
Chicago ·
MLA ·
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CSE |
Export
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Manager
APA (6th Edition):
Vargas, M. (2013). Nutrient Response and Aging in Invertebrate
Models. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:185790
Chicago Manual of Style (16th Edition):
Vargas, Miguel. “Nutrient Response and Aging in Invertebrate
Models.” 2013. Doctoral Dissertation, University of Manchester. Accessed March 07, 2021.
http://www.manchester.ac.uk/escholar/uk-ac-man-scw:185790.
MLA Handbook (7th Edition):
Vargas, Miguel. “Nutrient Response and Aging in Invertebrate
Models.” 2013. Web. 07 Mar 2021.
Vancouver:
Vargas M. Nutrient Response and Aging in Invertebrate
Models. [Internet] [Doctoral dissertation]. University of Manchester; 2013. [cited 2021 Mar 07].
Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:185790.
Council of Science Editors:
Vargas M. Nutrient Response and Aging in Invertebrate
Models. [Doctoral Dissertation]. University of Manchester; 2013. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:185790
Baylor University
12.
Thogmartin, Amanda K.
Investigation of the role of ipp-5 and lfe-2 in the IP3 signaling pathway in Caenorhabditis elegans ovulation.
Degree: MS, Biology., 2010, Baylor University
URL: http://hdl.handle.net/2104/7977
► C. elegans provides a useful system with which to study signaling pathways, giving information that can be applied to many organisms. The use of RNA…
(more)
▼ C.
elegans provides a useful system with which to study signaling pathways, giving information that can be applied to many organisms. The use of RNA interference can be used to study the genes involved in many different pathways, including the inositol triphosphate (IP3) signaling pathway. This pathway is involved in maintaining contractions necessary for C.
elegans ovulation. Using an RNAi feeding protocol, expression of several protein synthesis and cell signaling genes were knocked down, causing sterility in the wild-type worm. Sterility was rescued in mutants having a constitutively active IP3 receptor (itr-1 (sy290)), revealing that the genes were somehow involved in IP3 signaling. Use of worms with mutant backgrounds of ipp-5 and lfe-2, which are involved in negatively regulating IP3, showed that lfe-2 expression is solely in the spermatheca. When RNAi of ribosomal genes is performed in this mutant, sterility is able to be rescued.
Advisors/Committee Members: Lee, Myeongwoo. (advisor).
Subjects/Keywords: Caenorhabditis elegans.
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APA ·
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Export
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APA (6th Edition):
Thogmartin, A. K. (2010). Investigation of the role of ipp-5 and lfe-2 in the IP3 signaling pathway in Caenorhabditis elegans ovulation. (Masters Thesis). Baylor University. Retrieved from http://hdl.handle.net/2104/7977
Chicago Manual of Style (16th Edition):
Thogmartin, Amanda K. “Investigation of the role of ipp-5 and lfe-2 in the IP3 signaling pathway in Caenorhabditis elegans ovulation.” 2010. Masters Thesis, Baylor University. Accessed March 07, 2021.
http://hdl.handle.net/2104/7977.
MLA Handbook (7th Edition):
Thogmartin, Amanda K. “Investigation of the role of ipp-5 and lfe-2 in the IP3 signaling pathway in Caenorhabditis elegans ovulation.” 2010. Web. 07 Mar 2021.
Vancouver:
Thogmartin AK. Investigation of the role of ipp-5 and lfe-2 in the IP3 signaling pathway in Caenorhabditis elegans ovulation. [Internet] [Masters thesis]. Baylor University; 2010. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2104/7977.
Council of Science Editors:
Thogmartin AK. Investigation of the role of ipp-5 and lfe-2 in the IP3 signaling pathway in Caenorhabditis elegans ovulation. [Masters Thesis]. Baylor University; 2010. Available from: http://hdl.handle.net/2104/7977
Hong Kong University of Science and Technology
13.
Ji, Xianglin LIFS.
Nutrient dependent turnover of lipid droplet associated proteins.
Degree: 2015, Hong Kong University of Science and Technology
URL: http://repository.ust.hk/ir/Record/1783.1-94920
;
https://doi.org/10.14711/thesis-b1514897
;
http://repository.ust.hk/ir/bitstream/1783.1-94920/1/th_redirect.html
► Lipid droplets (LDs) are conserved organelles for cellular fat storage. In C.elegans, numerous LDs can be found in intestinal cells, where fat is primarily stored.…
(more)
▼ Lipid droplets (LDs) are conserved organelles for cellular fat storage. In C.elegans, numerous LDs can be found in intestinal cells, where fat is primarily stored. Proteomic studies have identified a large set of LD associated proteins. However, mechanisms governing the targeting and turnover of these proteins are largely unknown. Our lab has previously identified DGAT-2 as a LD associated protein in C.elegans. DGAT-2 is an acyl-coA:diacylglycerol acyltransferase that catalyzes the synthesis of triacylgclyerol, which is stored in LDs. DGAT-2 is localized to LDs when animals are actively feeding. However, DGAT-2 is undetectable in starved animals. In contrast, another LD associated protein, the short-chain dehydrogenase 3 (DHS-3), remains stable under the same condition. Our obervations indicate that there may be differential mechanisms for the turnover of LD associated proteins. In this study, I found that the degradation of DGAT-2 under starvation condition is regulated by the LD assoicated ancient ubiquitous protein 1 (AUP-1) in C. elegans. In addition, I found that AUP-1 may regulate the turnover of DGAT-2 through its interaction with components of the ERAD pathway. I propose that AUP-1 may recruit sepcific E2 and E3 enzymes to the LDs surface to ubiquitinate DGAT-2 in starved worms.
Subjects/Keywords: Lipids
; Metabolism
; Proteins
; Caenorhabditis elegans
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APA (6th Edition):
Ji, X. L. (2015). Nutrient dependent turnover of lipid droplet associated proteins. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-94920 ; https://doi.org/10.14711/thesis-b1514897 ; http://repository.ust.hk/ir/bitstream/1783.1-94920/1/th_redirect.html
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):
Ji, Xianglin LIFS. “Nutrient dependent turnover of lipid droplet associated proteins.” 2015. Thesis, Hong Kong University of Science and Technology. Accessed March 07, 2021.
http://repository.ust.hk/ir/Record/1783.1-94920 ; https://doi.org/10.14711/thesis-b1514897 ; http://repository.ust.hk/ir/bitstream/1783.1-94920/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ji, Xianglin LIFS. “Nutrient dependent turnover of lipid droplet associated proteins.” 2015. Web. 07 Mar 2021.
Vancouver:
Ji XL. Nutrient dependent turnover of lipid droplet associated proteins. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2015. [cited 2021 Mar 07].
Available from: http://repository.ust.hk/ir/Record/1783.1-94920 ; https://doi.org/10.14711/thesis-b1514897 ; http://repository.ust.hk/ir/bitstream/1783.1-94920/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ji XL. Nutrient dependent turnover of lipid droplet associated proteins. [Thesis]. Hong Kong University of Science and Technology; 2015. Available from: http://repository.ust.hk/ir/Record/1783.1-94920 ; https://doi.org/10.14711/thesis-b1514897 ; http://repository.ust.hk/ir/bitstream/1783.1-94920/1/th_redirect.html
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
California State University – East Bay
14.
Avina, Monika.
Cellular and Molecular Factors Influencing Mechanosensory Circuit Development in C.elegans.
Degree: 2016, California State University – East Bay
URL: http://hdl.handle.net/10211.3/164276
► In C. elegans, response to mechanical stimuli is mediated by two mechanosensory circuits. One circuit functions in the anterior to promote backward movement and another…
(more)
▼ In C.
elegans, response to mechanical stimuli is mediated by two mechanosensory circuits. One circuit functions in the anterior to promote backward movement and another circuit functions in the posterior to promote forward movement. The posterior neural circuit includes the mechanosensory neuron, PLM, which is required for detecting gentle touch within the posterior half of the animal. As expected for a spatially restricted function, the PLM dendrite extends from the tail and terminates just posterior to the anterior mechanosensory neuron, ALM. How is this termination point established? The cellular and molecular mechanisms that control this process are not well understood. I have used molecular genetics and microscopy to help identify these mechanisms.
Interestingly, the dendrite tip of PLM makes contact with the neurite tip of BDU, an interneuron. Moreover, genetic ablation of BDU using a mosaic analysis strategy lead to significant PLM overextension in comparison to controls (Gallegos lab unpublished). In these initial experiments BDU was not visible. To determine if BDU makes and maintains contact with PLM in control animals, we re-made the mosaic analysis strain to allow visualization of both BDU and PLM. I found that BDU makes contact with PLM only in 70% of the control animals. Moreover, overexpression of unc-86 transcription factor in the extrachromosomal array likely leads to BDU guidance defects. Finally, my characterization of a new experimental system involving an unc-86 free duplication instead of an extrachromosomal array does not exhibit these defects and is better suited to confirm the role of BDU in PLM termination.
I am also interested in molecular mechanisms that regulate PLM development. Importantly, sax-1 and sax-2 function cell autonomously to regulate PLM termination. cbk1, the sax-1 homolog in S. cerevisiae regulates cell growth and protein secretion via a rab GTPase, sec4. Interestingly, all three known mutant alleles of rab-10 (dx2, ok1494 and q373), a worm homolog of sec-4, are defective in endocytic recycling in C.
elegans intestine. However, in PLM, we find that while the null alleles (dx2, ok1494) result in PLM overextension, PLM neurite length in the missense allele, q373, is not significantly different from wild type. We hypothesize that the missense mutation in allele q373 does not affect the pathways involved in PLM termination. To test this hypothesis, I developed a genetic strategy to cross a randomly integrated transgene carrying rab-10 (q373) allele into homozygous rab-10 (ok1494) animals. Interestingly, I found that the missense allele, q373, of rab-10, fails to rescue the mutant phenotype (PLM overextension) of the deletion allele, ok1494. This result could likely be due to misexpression of the randomly integrated rab-10 (q373) transgene and the future characterization of the localization of transgene expression could help solve this question.
Advisors/Committee Members: Baysdorfer, Dr. Christoph W. (advisor), Gallegos, Dr. Maria E. (primaryAdvisor).
Subjects/Keywords: Caenorhabditis elegans – Nervous system
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APA (6th Edition):
Avina, M. (2016). Cellular and Molecular Factors Influencing Mechanosensory Circuit Development in C.elegans. (Thesis). California State University – East Bay. Retrieved from http://hdl.handle.net/10211.3/164276
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):
Avina, Monika. “Cellular and Molecular Factors Influencing Mechanosensory Circuit Development in C.elegans.” 2016. Thesis, California State University – East Bay. Accessed March 07, 2021.
http://hdl.handle.net/10211.3/164276.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Avina, Monika. “Cellular and Molecular Factors Influencing Mechanosensory Circuit Development in C.elegans.” 2016. Web. 07 Mar 2021.
Vancouver:
Avina M. Cellular and Molecular Factors Influencing Mechanosensory Circuit Development in C.elegans. [Internet] [Thesis]. California State University – East Bay; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10211.3/164276.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Avina M. Cellular and Molecular Factors Influencing Mechanosensory Circuit Development in C.elegans. [Thesis]. California State University – East Bay; 2016. Available from: http://hdl.handle.net/10211.3/164276
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Georgia
16.
Meyer, Dean Vallen.
Molecular mechanisms of action of nickel in the nematode Caenorhabditis elegans.
Degree: 2016, University of Georgia
URL: http://hdl.handle.net/10724/34465
► Caenorhabditis elegans is a bacterivorous nematode used as a model organism in biosciences research. Its characteristics make it suitable for toxicological investigations of environmental exposures.…
(more)
▼ Caenorhabditis elegans is a bacterivorous nematode used as a model organism in biosciences research. Its characteristics make it suitable for toxicological investigations of environmental exposures. It has been used extensively to assess the
effects of exposure to metals. Nickel is a ubiquitous metal present in the soil, air, and water, to which all living organisms are exposed daily. In this dissertation, the effects of nickel on C. elegans are examined, with particular emphasis on
characterizing cellular detoxification pathways involved in counteracting the effects of high concentrations of nickel. Pathways studied included metallothioneins, divalent metal transporters, a heat shock protein, an ABC transporter, phytochelatin, and
coelomocytes. In addition, this dissertation evaluated the differential toxicity of seven soluble nickel salts, and investigated whether nickel caused degeneration of cholinergic and dopaminergic pathways in C. elegans.
Subjects/Keywords: Nickel; Caenorhabditis elegans; detoxification
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APA (6th Edition):
Meyer, D. V. (2016). Molecular mechanisms of action of nickel in the nematode Caenorhabditis elegans. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/34465
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):
Meyer, Dean Vallen. “Molecular mechanisms of action of nickel in the nematode Caenorhabditis elegans.” 2016. Thesis, University of Georgia. Accessed March 07, 2021.
http://hdl.handle.net/10724/34465.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Meyer, Dean Vallen. “Molecular mechanisms of action of nickel in the nematode Caenorhabditis elegans.” 2016. Web. 07 Mar 2021.
Vancouver:
Meyer DV. Molecular mechanisms of action of nickel in the nematode Caenorhabditis elegans. [Internet] [Thesis]. University of Georgia; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10724/34465.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Meyer DV. Molecular mechanisms of action of nickel in the nematode Caenorhabditis elegans. [Thesis]. University of Georgia; 2016. Available from: http://hdl.handle.net/10724/34465
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
17.
Antonio Josà de Jesus Evangelista.
Efeito do bloqueio das proteÃnas hsp90 sobre a sensibilidade a antifÃngicos e produÃÃo de fatores de virulÃncia no complexo Cryptococcus neoformans/C. gattii.
Degree: Master, 2015, Universidade Federal do Ceará
URL: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=15073
;
► Cryptococcus neoformans species Complex comprises the main agents of cryptococcosis, an important systemic mycosis of nature and opportunistic. These species are capable of expressing multiple…
(more)
▼ Cryptococcus neoformans species Complex comprises the main agents of cryptococcosis, an important systemic mycosis of nature and opportunistic. These species are capable of expressing multiple virulence factors that contribute to the development of resistance to antifungal therapeutic use. Research seeking new effective therapy measures are necessary. Heat shock proteins (Hsp) have been shown to be a promising molecular target for medical treatment of various diseases such as various forms of cancer and atherosclerosis. Studies have demonstrated that the expression of these chaperonins is also required for the maintenance of cellular homeostasis in different fungal pathogens. From this perspective, this study aimed to investigate the effect of blocking the protein Hsp90 front of sensitivity to antifungal agents in vitro planktonic cells and sessile, production of virulence factors in vitro and in vivo virulence in Cryptococcus neoformans species Complex. Therefore, the action of yeast Hsp90 protein was blocked with radicicol drug - an antibiotic capable of inhibiting the ATPase activity of Hsp90 - and then the cultures were evaluated for in vitro susceptibility to antifungal agents for therapeutic use in planktonic cells and associated in biofilms. We also assessed the effect of inactivation of Hsp90 on the production of virulence factors capsule, melanin and proteases. In addition, the in vivo virulence was investigated in a model of experimental infection using the nematode Caenorhabditis elegans. The results revealed that radicicol inhibited the growth of planktonic cells Cryptococcus spp. (n=12) with values of minimum inhibitory concentration (MIC) ranging from 0.5 to 2 μg/mL. We observed synergy between pharmacological and radicicol azoles. Furthermore, blockade of Hsp90 potentiated the effect of in vitro antifungal agents, particularly for the fluconazole and itraconazole, which MIC values were reduced by up to 64 times the face of isolated cells (n=12). Although the blockade of Hsp90 by isolated radicicol was not able to inhibit biofilm formation and biofilm formed of Cryptococcus spp. (n=12) (p>0.05), the inactivation of Hsp90 potentiated the effect of amphotericin B, azoles, especially fluconazole, when tested in combination with radicicol (p<0.05). Moreover, blockade of Hsp90 significantly reduced the volume of capsular Cryptococcus spp. (n=4) (p<0.05). However, no difference was observed in production of melanin by radicicol treated cells (n=4) (p>0.05) as well as the production of protease by strains of Cryptococcus spp. (n=4) (p>0.05). By contrast, inactivation of Hsp90 decreased virulence Cryptococcus spp. in vitro and in vivo in C. elegans (p<0.0001) as well as maximize the effect of fluconazole in vitro and in vivo. Therefore, Hsp90 is an important target for the development of antifungal strategies. However, further studies are needed to better understand the role of Hsp90 in fungal pathogens of the genus Cryptococcus spp.
O Complexo Cryptococcus neoformans/C. gattii compreende os principais…
Advisors/Committee Members: Rossana de Aguiar Cordeiro, Marcos FÃbio Gadelha Rocha, Reginaldo GolÃalves de Lima Neto.
Subjects/Keywords: MICROBIOLOGIA MEDICA; Cryptococcus; Criptococose; Caenorhabditis elegans; Cryptococcus; cryptococcosis; Caenorhabditis elegans.
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APA (6th Edition):
Evangelista, A. J. d. J. (2015). Efeito do bloqueio das proteÃnas hsp90 sobre a sensibilidade a antifÃngicos e produÃÃo de fatores de virulÃncia no complexo Cryptococcus neoformans/C. gattii. (Masters Thesis). Universidade Federal do Ceará. Retrieved from http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=15073 ;
Chicago Manual of Style (16th Edition):
Evangelista, Antonio Josà de Jesus. “Efeito do bloqueio das proteÃnas hsp90 sobre a sensibilidade a antifÃngicos e produÃÃo de fatores de virulÃncia no complexo Cryptococcus neoformans/C. gattii.” 2015. Masters Thesis, Universidade Federal do Ceará. Accessed March 07, 2021.
http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=15073 ;.
MLA Handbook (7th Edition):
Evangelista, Antonio Josà de Jesus. “Efeito do bloqueio das proteÃnas hsp90 sobre a sensibilidade a antifÃngicos e produÃÃo de fatores de virulÃncia no complexo Cryptococcus neoformans/C. gattii.” 2015. Web. 07 Mar 2021.
Vancouver:
Evangelista AJdJ. Efeito do bloqueio das proteÃnas hsp90 sobre a sensibilidade a antifÃngicos e produÃÃo de fatores de virulÃncia no complexo Cryptococcus neoformans/C. gattii. [Internet] [Masters thesis]. Universidade Federal do Ceará 2015. [cited 2021 Mar 07].
Available from: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=15073 ;.
Council of Science Editors:
Evangelista AJdJ. Efeito do bloqueio das proteÃnas hsp90 sobre a sensibilidade a antifÃngicos e produÃÃo de fatores de virulÃncia no complexo Cryptococcus neoformans/C. gattii. [Masters Thesis]. Universidade Federal do Ceará 2015. Available from: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=15073 ;
Ryerson University
18.
Yee, Callista Stephanie.
ENU-3 is a novel outgrowth and guidance protein in c. elegans.
Degree: 2011, Ryerson University
URL: https://digital.library.ryerson.ca/islandora/object/RULA%3A1044
► During the development of the nervous system, the migration of many cells and axons is guided by extracellular molecules. These molecules bind to receptors at…
(more)
▼ During the development of the nervous system, the migration of many cells and axons is guided by extracellular molecules. These molecules bind to receptors at the tips of the growth cones of migrating axons and trigger intracellular signalling to steer the axons along the correct trajectories. Previous work has identified a novel mutant, enu-3 (enhancer of Unc), that enhances the motor neuron axon outgrowth defects observed in strains of
Caenorhabditis elegans that lack either the UNC-5 receptor or its ligand UNC-6/Netrin, enu-3 single mutants have weak motor neuron axon migration defects. Both outgrowth defects of double mutants and axon migration defects of enu-3 mutants were rescued by expression of the H04D03.1 gene product. Enu-3/H04D03.1 encodes a novel predicted putative trans-membrane protein of 204 amino acids. ENU-3 is expressed weakly expressed in many cell bodies along the ventral cord, including those of the DA and DB motor neurons.
Advisors/Committee Members: Killeen, Marie (Thesis advisor), Ryerson University (Degree grantor).
Subjects/Keywords: Caenorhabditis Elegans – Genetics; Caenorhabditis Elegans; Molecular biology; Ryerson University – Dissertations
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APA (6th Edition):
Yee, C. S. (2011). ENU-3 is a novel outgrowth and guidance protein in c. elegans. (Thesis). Ryerson University. Retrieved from https://digital.library.ryerson.ca/islandora/object/RULA%3A1044
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):
Yee, Callista Stephanie. “ENU-3 is a novel outgrowth and guidance protein in c. elegans.” 2011. Thesis, Ryerson University. Accessed March 07, 2021.
https://digital.library.ryerson.ca/islandora/object/RULA%3A1044.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Yee, Callista Stephanie. “ENU-3 is a novel outgrowth and guidance protein in c. elegans.” 2011. Web. 07 Mar 2021.
Vancouver:
Yee CS. ENU-3 is a novel outgrowth and guidance protein in c. elegans. [Internet] [Thesis]. Ryerson University; 2011. [cited 2021 Mar 07].
Available from: https://digital.library.ryerson.ca/islandora/object/RULA%3A1044.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Yee CS. ENU-3 is a novel outgrowth and guidance protein in c. elegans. [Thesis]. Ryerson University; 2011. Available from: https://digital.library.ryerson.ca/islandora/object/RULA%3A1044
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Texas Southwestern Medical Center
19.
Yoshimoto, Jennifer Ann Winn.
Identification and Characterization of EFL-3, a C. Elegans E2F Transcription Factor.
Degree: 2011, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/954
► The development of an organism depends on cells receiving and executing their specific fates, though how this process is regulated remains largely unknown. Here, we…
(more)
▼ The development of an organism depends on cells receiving and executing their specific fates, though how this process is regulated remains largely unknown. Here, we identify a mechanism by which a specific cell fate, apoptosis, is determined through the cooperative efforts of Hox and E2F proteins. E2F transcription factors are critical, conserved regulators of the cell cycle and apoptosis. However, little is known about the two most recently discovered mammalian E2Fs—-E2F7 and E2F8. In the nematode
Caenorhabditis elegans, we identify a novel E2F7/8 homolog, EFL-3, and show that EFL-3 functions cooperatively with LIN-39, providing the first example in which these two major developmental pathways—-E2F and Hox—-are able to directly regulate the same target gene. Our studies demonstrate that LIN-39 and EFL-3 function in a cell type-specific context to regulate transcription of the egl-1 BH3 only cell death gene and determine cell fate during development.
Advisors/Committee Members: Avery, Leon.
Subjects/Keywords: Caenorhabditis elegans; E2F Transcription Factors; Caenorhabditis elegans Proteins
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APA (6th Edition):
Yoshimoto, J. A. W. (2011). Identification and Characterization of EFL-3, a C. Elegans E2F Transcription Factor. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/954
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):
Yoshimoto, Jennifer Ann Winn. “Identification and Characterization of EFL-3, a C. Elegans E2F Transcription Factor.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021.
http://hdl.handle.net/2152.5/954.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Yoshimoto, Jennifer Ann Winn. “Identification and Characterization of EFL-3, a C. Elegans E2F Transcription Factor.” 2011. Web. 07 Mar 2021.
Vancouver:
Yoshimoto JAW. Identification and Characterization of EFL-3, a C. Elegans E2F Transcription Factor. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2152.5/954.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Yoshimoto JAW. Identification and Characterization of EFL-3, a C. Elegans E2F Transcription Factor. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/954
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
20.
Goudeau, Jérôme.
Links between Germline and Longevity in Caenorhabditis elegans : Étude des mécanismes moléculaires liant la lignée germinale au vieillissement chez Caenorhabditis elegans.
Degree: Docteur es, Sciences de la vie, 2011, Lyon, École normale supérieure
URL: http://www.theses.fr/2011ENSL0641
► Un nouveau gène de la longévité ouvre de nouvelles pistes pour vieillir mieux. L'accroissement de la longévité induit par la suppression des tissus reproducteurs a…
(more)
▼ Un nouveau gène de la longévité ouvre de nouvelles pistes pour vieillir mieux. L'accroissement de la longévité induit par la suppression des tissus reproducteurs a été observé chez la drosophile et chez le ver. Chez ce dernier, l'opération lui donne 60% de vie en plus et lui permet un vieillissement harmonieux et en bonne santé. Les mécanismes moléculaires qui induisent cette réponse font l'objet d'intenses recherches. Certains gènes étaient déjà connus pour être associés à l'accroissement de la longévité des vers sans lignée germinale, et nous avons démontré l'existence d'une nouvelle voie impliquant le récepteur nucléaire NHR-80. Les nématodes dépourvus de lignée germinale et dont nhr-80 est muté ne voient pas leur longévité augmenter. En outre, la surexpression du gène allonge davantage leur durée de vie: elle est 150% plus longue que celle de leurs congénères sauvages. Cela démontre l'importance de ce récepteur nucléaire dont l'activation par une hormone encore inconnue enclenche l'expression ou la mise sous silence de centaines d'autres gènes. Notamment, nous avons montré que l'une des cibles de NHR-80, l'enzyme FAT-6 qui transforme l'acide stéarique en acide oléique est fondamentale, puisque les vers dépourvus de lignée germinale ne présentent plus aucun gain en longévité en l'absence de FAT-6. À terme, nous espérons pouvoir récapituler les effets de l'ablation de la lignée germinale chez un organisme fertile, c'est à dire, d'induire les réarrangements métaboliques qui ont lieu suite à cette opération afin d'en tirer les effets positifs sur la santé, sans affecter la reproduction.
Discovery of a key longevity gene opens new perspectives for healthy aging.Increased longevity induced by reproductive tissues removal (germline ablation) is observed in the fly Drosophila melanogaster and in the worm Caenorhabditis elegans. In the latter, the operation increases lifespan by 60%, and enables the nematode to age harmoniously and in good health. The molecular mechanisms that induce this response are subject of intensive research. Our study reveals the existence of a new powerful longevity gene, nhr-80, which mediates this longevity effect. We have shown that inactivation of nhr-80 prevents lifespan increase. Furthermore, nhr-80 overexpression lengthens the nematodes' lifespan by 150%! nhr-80 encodes a nuclear receptor, which activation by a still unknown hormone controls the expression of hundreds of other genes. We showed that one of the critical NHR-80 targets, the enzyme FAT-6, which transforms stearic acid into oleic acid, is necessary to prolong lifespan since a mutation of the fat-6 gene suppresses the effects of germline ablation on longevity. The next step will be to determine how an increase in the level of oleic acid induces an adaptive response resulting in increased longevity. This research may lead to the exciting possibility of recapitulating the benefits of germline ablation in fertile animals; in other words, to activate the longevity effects normally triggered by germline ablation in order to fight,…
Advisors/Committee Members: Aguilaniu, Hugo (thesis director).
Subjects/Keywords: Caenorhabditis elegans; Aging; Rejuvenation; Proteasome; Reproduction; Caenorhabditis elegans
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APA (6th Edition):
Goudeau, J. (2011). Links between Germline and Longevity in Caenorhabditis elegans : Étude des mécanismes moléculaires liant la lignée germinale au vieillissement chez Caenorhabditis elegans. (Doctoral Dissertation). Lyon, École normale supérieure. Retrieved from http://www.theses.fr/2011ENSL0641
Chicago Manual of Style (16th Edition):
Goudeau, Jérôme. “Links between Germline and Longevity in Caenorhabditis elegans : Étude des mécanismes moléculaires liant la lignée germinale au vieillissement chez Caenorhabditis elegans.” 2011. Doctoral Dissertation, Lyon, École normale supérieure. Accessed March 07, 2021.
http://www.theses.fr/2011ENSL0641.
MLA Handbook (7th Edition):
Goudeau, Jérôme. “Links between Germline and Longevity in Caenorhabditis elegans : Étude des mécanismes moléculaires liant la lignée germinale au vieillissement chez Caenorhabditis elegans.” 2011. Web. 07 Mar 2021.
Vancouver:
Goudeau J. Links between Germline and Longevity in Caenorhabditis elegans : Étude des mécanismes moléculaires liant la lignée germinale au vieillissement chez Caenorhabditis elegans. [Internet] [Doctoral dissertation]. Lyon, École normale supérieure; 2011. [cited 2021 Mar 07].
Available from: http://www.theses.fr/2011ENSL0641.
Council of Science Editors:
Goudeau J. Links between Germline and Longevity in Caenorhabditis elegans : Étude des mécanismes moléculaires liant la lignée germinale au vieillissement chez Caenorhabditis elegans. [Doctoral Dissertation]. Lyon, École normale supérieure; 2011. Available from: http://www.theses.fr/2011ENSL0641
Columbia University
21.
Gordon, Patricia Marie.
A Competition Mechanism for a Homeotic Neuron Identity Transformation in Caenorhabditis Elegans.
Degree: 2015, Columbia University
URL: https://doi.org/10.7916/D87H1H90
► As embryos proceed through development, they must undergo a series of cell fate decisions. At each division, potency is progressively restricted until a terminally differentiated,…
(more)
▼ As embryos proceed through development, they must undergo a series of cell fate decisions. At each division, potency is progressively restricted until a terminally differentiated, postmitotic cell is produced. An important part of that cell type determination is repression of alternative fate possibilities. In this thesis, I have explored the mechanisms by which a single transcription factor activates certain cell fates while inhibiting others, using the Caenorhabditis elegans ALM and BDU neurons as a model. ALM neuron identity is regulated by two interacting transcription factors: the POU homeobox gene unc-86 and the LIM homeobox gene mec-3. I investigated fate determination in BDU neurons, the sister cells of ALM. I found that BDU identity is broadly defined by a combination of unc-86 and the Zn finger transcription factor pag-3, while the neuropeptidergic subroutine of BDU is determined by the LIM homeobox gene ceh-14. In addition, I found that reciprocal homeotic transformations occur between ALM and BDU neurons upon loss of either mec-3 or pag-3. In mec-3 mutants, ALM neurons acquire the gene expression profile and morphological characteristics of BDU cells, while in pag-3 mutants, BDU neurons express genes normally found in ALM and change some aspects of their morphology to resemble ALM. While these fate switches appear to be a simple case of cross-repression, the mechanism is in fact more complicated, as pag-3 is expressed not just in BDU but also in ALM. In this thesis, I present evidence that MEC-3 inhibits execution of BDU identity in ALM by physically binding to UNC-86 and sequestering it away from the promoters of BDU genes. This work expands upon the literature examining simultaneous activation of one identity program and repression of alternate programs by introducing a novel mechanism by which a transcription factor competes to direct specific cell fates.
Subjects/Keywords: Caenorhabditis elegans; Caenorhabditis elegans – Genetics; Cell division; Cell differentiation; Homeobox genes
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APA (6th Edition):
Gordon, P. M. (2015). A Competition Mechanism for a Homeotic Neuron Identity Transformation in Caenorhabditis Elegans. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D87H1H90
Chicago Manual of Style (16th Edition):
Gordon, Patricia Marie. “A Competition Mechanism for a Homeotic Neuron Identity Transformation in Caenorhabditis Elegans.” 2015. Doctoral Dissertation, Columbia University. Accessed March 07, 2021.
https://doi.org/10.7916/D87H1H90.
MLA Handbook (7th Edition):
Gordon, Patricia Marie. “A Competition Mechanism for a Homeotic Neuron Identity Transformation in Caenorhabditis Elegans.” 2015. Web. 07 Mar 2021.
Vancouver:
Gordon PM. A Competition Mechanism for a Homeotic Neuron Identity Transformation in Caenorhabditis Elegans. [Internet] [Doctoral dissertation]. Columbia University; 2015. [cited 2021 Mar 07].
Available from: https://doi.org/10.7916/D87H1H90.
Council of Science Editors:
Gordon PM. A Competition Mechanism for a Homeotic Neuron Identity Transformation in Caenorhabditis Elegans. [Doctoral Dissertation]. Columbia University; 2015. Available from: https://doi.org/10.7916/D87H1H90
Hong Kong University of Science and Technology
22.
Tam, Chung Nga.
The role of ram-2 in Caenorhabditis elegans development.
Degree: 2004, Hong Kong University of Science and Technology
URL: http://repository.ust.hk/ir/Record/1783.1-3905
;
https://doi.org/10.14711/thesis-b818116
;
http://repository.ust.hk/ir/bitstream/1783.1-3905/1/th_redirect.html
► C. elegans male tail is a structurally complex organ for locating the hermaphrodite's vulva in mating. The morphogenesis of its constituent sensory rays is a…
(more)
▼ C. elegans male tail is a structurally complex organ for locating the hermaphrodite's vulva in mating. The morphogenesis of its constituent sensory rays is a complex process tightly under genetic control. Mutations of a number of ram loci have been shown to result in abnormal ray morphology. ram (bx32) mutants have the most severe Ram phenotype whereas the rays are so swollen that individual rays cannot be distinguished . Another ram mutation, ram-2 (bx39ts) with a milder Ram phenotype, initially defined by mapping as a separate locus on LG II, has now been confirmed as allelic to ram (bx32). The bx32 allele of ram-2 was generated by EMS. I showed that ram-2 indeed encodes a cuticular collagen. It has a single nucleotide changed resulting in substitution of the glycine 126 by a glutamic acid. This mutation is at the first Gly-X-Y domain. While homozygous bx32 or bx32/Df mutants displayed the most severe Ram phenotype, it was initially interpreted to be a null allele. However, this bx32 allele presented a temperature sensitive phenotype in heterozygosity. The rays of bx32/+ animals had severely swollen ray tips at 25°C but not as serious at 20°C. Since this phenotype was not observed in +/mnDf83 (with the ram-2 locus deleted), we propose that bx32 acts as a temperature sensitive dominant negative allele instead of being a null allele. This idea was further supported by the results of interactions of ram-2 with other collagen genes and the ram-2 knockdown experiments with dsRNA. bx32 mutation alone was found to affect ray cell migration. This defect was enhanced by the ev400 allele of unc-6 netrin. In addition, the interaction between ram-2 and unc-5 or unc-6 was also observed in embryos. Double mutations could dramatically reduce the brood size, or had the brood size restored in specific alleles combination. Based on these findings, we hypothesized that RAM-2 is an extracellular matrix component, which plays an important role in both ray morphogenesis and early embryonic function, both of which may be brought about by abnormality in cellular migration.
Subjects/Keywords: Caenorhabditis elegans
; Caenorhabditis elegans – Genetics
; Caenorhabditis elegans – Morphogenesis
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APA (6th Edition):
Tam, C. N. (2004). The role of ram-2 in Caenorhabditis elegans development. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-3905 ; https://doi.org/10.14711/thesis-b818116 ; http://repository.ust.hk/ir/bitstream/1783.1-3905/1/th_redirect.html
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):
Tam, Chung Nga. “The role of ram-2 in Caenorhabditis elegans development.” 2004. Thesis, Hong Kong University of Science and Technology. Accessed March 07, 2021.
http://repository.ust.hk/ir/Record/1783.1-3905 ; https://doi.org/10.14711/thesis-b818116 ; http://repository.ust.hk/ir/bitstream/1783.1-3905/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Tam, Chung Nga. “The role of ram-2 in Caenorhabditis elegans development.” 2004. Web. 07 Mar 2021.
Vancouver:
Tam CN. The role of ram-2 in Caenorhabditis elegans development. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2004. [cited 2021 Mar 07].
Available from: http://repository.ust.hk/ir/Record/1783.1-3905 ; https://doi.org/10.14711/thesis-b818116 ; http://repository.ust.hk/ir/bitstream/1783.1-3905/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Tam CN. The role of ram-2 in Caenorhabditis elegans development. [Thesis]. Hong Kong University of Science and Technology; 2004. Available from: http://repository.ust.hk/ir/Record/1783.1-3905 ; https://doi.org/10.14711/thesis-b818116 ; http://repository.ust.hk/ir/bitstream/1783.1-3905/1/th_redirect.html
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Utah
23.
Barusch, Nathaniel Morris.
Linking synaptotagmin to vesicle fusion.
Degree: Honors BFA;, Biology;, 2009, University of Utah
URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/326/rec/708
► Synaptotagmin 1 is an integral synaptic vesicle protein and is believed to be the major calcium sensor in synaptic vesicle fusion. Loss of synaptotagmin 1…
(more)
▼ Synaptotagmin 1 is an integral synaptic vesicle protein and is believed to be the major calcium sensor in synaptic vesicle fusion. Loss of synaptotagmin 1 from the nematode C. elegans results in an uncoordinated phenotype and decreased levels of neurotransmitter release. Synaptotagmin consists of two calcium/lipid binding C2 domains (C2A and C2B) separated by a short flexible linker (12 AA). While the role of the C2 domains has been extensively studied, the role of the short linker domain between them has not. It has been proposed that the linker sequence may be important in interacting with the SNAREs and with positioning the C2 domains in relation to each other and the SNARE complex. We explore two models for the role of the linker domain. 1) The sequence of the linker is important for function. To test the effects of the linker sequence the sequence was replaced with a flexible sequence consisting of repeats of glycine-glycine-serine (GGS). 2) The length of the linker is critical for its function. To test the effects of increasing the length of this linker domain the sequence was repeated, doubling the length. Initial results show partial rescue of endocytosis and exocytosis function for the flexible and double linker constructs. This suggests the sequence and length of the linker is important, but not vital, for synaptotagmin function. The next step is to determine whether endocytosis or exocytosis is being affected by these mutations.
Subjects/Keywords: Caenorhabditis elegans; Synaptic vesicles; Neural transmission
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APA (6th Edition):
Barusch, N. M. (2009). Linking synaptotagmin to vesicle fusion. (Masters Thesis). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/326/rec/708
Chicago Manual of Style (16th Edition):
Barusch, Nathaniel Morris. “Linking synaptotagmin to vesicle fusion.” 2009. Masters Thesis, University of Utah. Accessed March 07, 2021.
http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/326/rec/708.
MLA Handbook (7th Edition):
Barusch, Nathaniel Morris. “Linking synaptotagmin to vesicle fusion.” 2009. Web. 07 Mar 2021.
Vancouver:
Barusch NM. Linking synaptotagmin to vesicle fusion. [Internet] [Masters thesis]. University of Utah; 2009. [cited 2021 Mar 07].
Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/326/rec/708.
Council of Science Editors:
Barusch NM. Linking synaptotagmin to vesicle fusion. [Masters Thesis]. University of Utah; 2009. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/326/rec/708
University of Utah
24.
Han, Hsiao-Fen.
Dissecting the Role of ALP-1 and EAT-1 Proteins in Regulation of Muscle Structure and Function.
Degree: PhD, Oncological Sciences, 2010, University of Utah
URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/7/rec/354
► The purpose of this dissertation is to define how muscle cells maintain their contractile machinery and how a rhythmic muscle contraction is regulated. These studies…
(more)
▼ The purpose of this dissertation is to define how muscle cells maintain their contractile machinery and how a rhythmic muscle contraction is regulated. These studies employed C. elegans as a model system to characterize pathways required for normal muscle structure and function. With easy manipulation and a wide variety of genetic tools, C. elegans is a powerful and efficient system to study gene function and to dissect underlying molecular mechanisms. In the first part of this dissertation, Z-disc-associated muscle proteins of the ALPEnigma family were characterized. The alp-1 gene in C. elegans encodes multiple ALPEnigma proteins. The ALP-1 proteins are broadly expressed at actin-anchorage sites, and play a role in maintaining actin filament organization within muscles. Genetic analysis revealed that ALP-1 and alpha-actinin act together to support the integrity of actin cytoarchitecture. The second part of this dissertation is focused on the characterization of the eat-1 gene in C. elegans. Mutations in eat-1 cause defects in the rhythmic contraction of the pharynx, an organ in the C. elegans digestive tract that is comprised of muscle, neuronal and epithelial cells, eat-1 encodes adenosine kinase, an evolutionarily conserved enzyme that catalyzes adenosine to adenosine monophosphate. Molecular and genetic studies showed that EAT-1 acts noncell autonomously and modulates adenosine receptormediated signaling to regulate pharyngeal muscle contraction. The studies reveal the important role of ALP-Enigma proteins in maintaining muscle structural integrity, and of adenosine kinase in regulating rhythmic muscle contraction, enhancing our knowledge of how muscle cells maintain their structure and contract properly.
Subjects/Keywords: Muscle Contraction; Muscle Proteins; Caenorhabditis elegans
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APA (6th Edition):
Han, H. (2010). Dissecting the Role of ALP-1 and EAT-1 Proteins in Regulation of Muscle Structure and Function. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/7/rec/354
Chicago Manual of Style (16th Edition):
Han, Hsiao-Fen. “Dissecting the Role of ALP-1 and EAT-1 Proteins in Regulation of Muscle Structure and Function.” 2010. Doctoral Dissertation, University of Utah. Accessed March 07, 2021.
http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/7/rec/354.
MLA Handbook (7th Edition):
Han, Hsiao-Fen. “Dissecting the Role of ALP-1 and EAT-1 Proteins in Regulation of Muscle Structure and Function.” 2010. Web. 07 Mar 2021.
Vancouver:
Han H. Dissecting the Role of ALP-1 and EAT-1 Proteins in Regulation of Muscle Structure and Function. [Internet] [Doctoral dissertation]. University of Utah; 2010. [cited 2021 Mar 07].
Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/7/rec/354.
Council of Science Editors:
Han H. Dissecting the Role of ALP-1 and EAT-1 Proteins in Regulation of Muscle Structure and Function. [Doctoral Dissertation]. University of Utah; 2010. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/7/rec/354
Georgia Tech
25.
Porto, Daniel Akashi.
Integrated computer vision and microscopy tools for all-optical interrogation of the nervous and muscular systems in Caenorhabditis elegans.
Degree: PhD, Electrical and Computer Engineering, 2018, Georgia Tech
URL: http://hdl.handle.net/1853/62243
► All animals constantly process sensory information from the environment to guide behavioral responses. A fundamental question in neuroscience is to understand how the nervous system…
(more)
▼ All animals constantly process sensory information from the environment to guide behavioral responses. A fundamental question in neuroscience is to understand how the nervous system uses neuronal circuits to perform neuronal computations between environmental signals and behavioral outputs, or in terms of systems analysis, what are transfer functions that describe this system’s function? A key challenge in answering this question in humans is the overwhelming complexity of the human brain. Furthermore, technical challenges limit the capabilities and accuracy of measurements of neuronal activity and behavioral outputs while simultaneously probing parts of the circuit.
Caenorhabditis elegans is a model organism with a small nervous system consisting of only 302 neurons, and has allowed for the elucidation of genetic and circuit mechanisms of neuronal computations. Additionally, advancements in experimental methodologies such as calcium imaging, optogenetics, and behavior tracking have enabled robust experimentation and analysis. However, conventional instrumentation used to perform these experiments are limited in the integration of these tools and analytical frameworks for extracted data. This thesis focuses on the development of several integrated platforms to perform optical interrogation of various aspects of the nervous system. I use image processing techniques and microscopy tools to improve the throughput and robustness of both experimentation and analysis. These platforms were implemented to address specific biological questions, and were used in experiments involving phenotyping morphology, measuring neuronal activity using functional imaging, activation of excitable cells using optogenetics, and behavior tracking using computer vision techniques. Using these platforms, I developed a reverse correlation methodology to systematically inspect the mechanosensation circuit in C.
elegans. I elucidate linear and nonlinear transformations that characterize the temporal and spatial properties of the neural circuitry, providing models that can predict its function. In another application, I used the developed platforms to perform FRET imaging of muscles in freely moving animals. This enabled the investigation of conformational changes of the muscle protein twitchin in vivo. In addition to these two biological investigations, I applied the developed techniques to address other limitations in C.
elegans research, including robust calcium imaging analysis in microfluidic devices, as well high-throughput screens for a spinal muscular atrophy model and a lipid storage mutant model. Together, the newly developed platforms and analysis pipelines have improved our ability to investigate activities and functions of neural circuits, and have enabled novel insights about the nervous and muscular systems of C.
elegans.
Advisors/Committee Members: Lu, Hang (advisor), McGrath, Patrick (advisor), Butera, Robert (advisor), Ting, Lena (advisor), Berman, Gordon (advisor).
Subjects/Keywords: Caenorhabditis elegans; Optogenetics; Calcium imaging; Behavior
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APA (6th Edition):
Porto, D. A. (2018). Integrated computer vision and microscopy tools for all-optical interrogation of the nervous and muscular systems in Caenorhabditis elegans. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/62243
Chicago Manual of Style (16th Edition):
Porto, Daniel Akashi. “Integrated computer vision and microscopy tools for all-optical interrogation of the nervous and muscular systems in Caenorhabditis elegans.” 2018. Doctoral Dissertation, Georgia Tech. Accessed March 07, 2021.
http://hdl.handle.net/1853/62243.
MLA Handbook (7th Edition):
Porto, Daniel Akashi. “Integrated computer vision and microscopy tools for all-optical interrogation of the nervous and muscular systems in Caenorhabditis elegans.” 2018. Web. 07 Mar 2021.
Vancouver:
Porto DA. Integrated computer vision and microscopy tools for all-optical interrogation of the nervous and muscular systems in Caenorhabditis elegans. [Internet] [Doctoral dissertation]. Georgia Tech; 2018. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1853/62243.
Council of Science Editors:
Porto DA. Integrated computer vision and microscopy tools for all-optical interrogation of the nervous and muscular systems in Caenorhabditis elegans. [Doctoral Dissertation]. Georgia Tech; 2018. Available from: http://hdl.handle.net/1853/62243
Vanderbilt University
26.
Nguyen, Thuy Tuong.
Oxidative stress in C. elegans: Discovery of a mechanistic role for gamma-ketoaldehyde lipid peroxidation products in the Free Radical Theory of Aging.
Degree: PhD, Pharmacology, 2016, Vanderbilt University
URL: http://hdl.handle.net/1803/14699
► Highly reactive acyclic levuglandin-like gamma-ketoaldehydes (gamma-KA, isoketals, or IsoKs) are formed as products of the isoprostane pathway of lipid peroxidation. IsoKs are known to covalently…
(more)
▼ Highly reactive acyclic levuglandin-like gamma-ketoaldehydes (gamma-KA, isoketals, or IsoKs) are formed as products of the isoprostane pathway of lipid peroxidation. IsoKs are known to covalently adduct ε-amino groups in lysyl residues of proteins, forming stable adducts and intramolecular cross-links. Increased IsoK-lysyl-lactam adducts are found in a number of disease conditions, including atherosclerosis, end-stage renal disease, and Alzheimer’s disease. A selective IsoK scavenger, salicylamine (SA), was developed and tested in
Caenorhabditis elegans to probe the pathophysiological processes in IsoK-mediated oxidative injury, and consequently provide the groundwork for the development of new rational therapeutic interventions to limit oxidative damage. Administration of SA extends adult nematode longevity by nearly 56% and prevents multiple deleterious age-related biochemical and functional changes. Testing of a variety of molecular targets for SA’s action revealed the sirtuin SIR-2.1 as the leading candidate. When SA was administered to a SIR-2.1 knockout strain, the effects on lifespan and healthspan extension were abolished. The SIR-2.1-dependent effects of SA were not mediated by large changes in gene expression programs or by significant changes in mitochondrial function. However, expression array analysis did show SA-dependent regulation of the transcription factor ets-7 and associated genes. In ets-7 knockout worms, SA’s longevity effects were abolished, similar to sir-2.1 knockouts. However, SA dose-dependently increases ets-7 mRNA levels in non-functional SIR-2.1 mutant, suggesting that both are necessary for SA’s complete lifespan and healthspan extension.
Advisors/Committee Members: L. Jackson Roberts, II (committee member), Michael Aschner (committee member), Sean Davies (committee member), Michael Freeman (committee member), John Oates (Committee Chair).
Subjects/Keywords: isoketals; aging; Caenorhabditis elegans; sirtuins; isoprostanes
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APA (6th Edition):
Nguyen, T. T. (2016). Oxidative stress in C. elegans: Discovery of a mechanistic role for gamma-ketoaldehyde lipid peroxidation products in the Free Radical Theory of Aging. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14699
Chicago Manual of Style (16th Edition):
Nguyen, Thuy Tuong. “Oxidative stress in C. elegans: Discovery of a mechanistic role for gamma-ketoaldehyde lipid peroxidation products in the Free Radical Theory of Aging.” 2016. Doctoral Dissertation, Vanderbilt University. Accessed March 07, 2021.
http://hdl.handle.net/1803/14699.
MLA Handbook (7th Edition):
Nguyen, Thuy Tuong. “Oxidative stress in C. elegans: Discovery of a mechanistic role for gamma-ketoaldehyde lipid peroxidation products in the Free Radical Theory of Aging.” 2016. Web. 07 Mar 2021.
Vancouver:
Nguyen TT. Oxidative stress in C. elegans: Discovery of a mechanistic role for gamma-ketoaldehyde lipid peroxidation products in the Free Radical Theory of Aging. [Internet] [Doctoral dissertation]. Vanderbilt University; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1803/14699.
Council of Science Editors:
Nguyen TT. Oxidative stress in C. elegans: Discovery of a mechanistic role for gamma-ketoaldehyde lipid peroxidation products in the Free Radical Theory of Aging. [Doctoral Dissertation]. Vanderbilt University; 2016. Available from: http://hdl.handle.net/1803/14699
Queens University
27.
Barnay, Rawah.
The Roles of the Neuropeptide Receptor NPR-14 in the Regulation of Sleep Behaviours in Caenorhabditis elegans
.
Degree: Biology, Queens University
URL: http://hdl.handle.net/1974/25859
► Most animals with a nervous system exhibit sleep behaviour(s) during their life cycle, which appears as a decreased level of physical activity and changes in…
(more)
▼ Most animals with a nervous system exhibit sleep behaviour(s) during their life cycle, which appears as a decreased level of physical activity and changes in metabolism. Even animals with a simple nervous system like Caenorhabditis elegans have shown sleep behaviour. Two types of sleep have been characterized in C. elegans. The first is a developmentally timed quiescence (DTS), known as lethargus; and the second is a stress induced quiescence (SIS). Each type of sleep functions through different neuronal pathways and utilizes a variety of neuropeptide signaling molecules. The DTS pathway uses the expression of the neuropeptide gene nlp-22 and that of the SIS pathway uses the neuropeptide flp-13. Our lab has discovered a neuropeptide receptor gene called npr-14 that, when mutated, displays quiescence behaviour. We seek to answer the question: How does npr-14 fit in the DTS or SIS sleep pathways? The role of npr-14 in the sleep circuit was tested using experiments that analyze the behaviour of npr-14 (LF) (loss of function) and npr-14(OE)(overexpression) alone and in combination with loss of function alleles of - flp-13, nlp-22, and other known components in the sleep pathway. Results of this research will enhance our understanding of the sleep circuit in C. elegans. Understanding this sleep circuit is important because it may contribute to the understanding of many sleep disorders.
Subjects/Keywords: Caenorhabditis elegans
;
sleep
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APA (6th Edition):
Barnay, R. (n.d.). The Roles of the Neuropeptide Receptor NPR-14 in the Regulation of Sleep Behaviours in Caenorhabditis elegans
. (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/25859
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Barnay, Rawah. “The Roles of the Neuropeptide Receptor NPR-14 in the Regulation of Sleep Behaviours in Caenorhabditis elegans
.” Thesis, Queens University. Accessed March 07, 2021.
http://hdl.handle.net/1974/25859.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Barnay, Rawah. “The Roles of the Neuropeptide Receptor NPR-14 in the Regulation of Sleep Behaviours in Caenorhabditis elegans
.” Web. 07 Mar 2021.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Vancouver:
Barnay R. The Roles of the Neuropeptide Receptor NPR-14 in the Regulation of Sleep Behaviours in Caenorhabditis elegans
. [Internet] [Thesis]. Queens University; [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1974/25859.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
Council of Science Editors:
Barnay R. The Roles of the Neuropeptide Receptor NPR-14 in the Regulation of Sleep Behaviours in Caenorhabditis elegans
. [Thesis]. Queens University; Available from: http://hdl.handle.net/1974/25859
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
University of Texas Southwestern Medical Center
28.
Wu, Cheng-Yang.
Using C. Elegans as Model Organism to Study the Mode of Action of a Natural Toxin, Psymberin.
Degree: 2011, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/956
► Psymberin is an extremely potent cytotoxin isolated from the marine sponges Psammocinia and Ircinia ramose. Several cancer cell lines are sensitive to psymberin, including breast,…
(more)
▼ Psymberin is an extremely potent cytotoxin isolated from the marine sponges Psammocinia and Ircinia ramose. Several cancer cell lines are sensitive to psymberin, including breast, melanoma and colon cancer cell lines. Psymberin is the only member of the pederin natural product family that contains a dihydroisocoumarin side chain. The cytotoxicities of psymberin in various human tumor cell lines are between sub-nanomolar to nanomolar IC50. Like pederin, the first member of this natural product family, psymberin and mycalamide A inhibit translation in vivo and in vitro. This inhibition by psymberin is 40 to 100 fold more potent than cycloheximide, which inhibits >90% translation at 100 micromolar in vivo. In a SAR study, both the cytotoxicity of psymberin and psymberin-induced translation inhibition were attenuated by substituting the psymberin side chain with the pederin side chain. However, the attenuation of cytotoxicity was relatively greater than of translation. The stereo configuration and both side chains of psymberin are required for both inhibition of translation and cytotoxicity. The result of the SAR study suggests that additional bioactivity is contained in psymberin. Psymberin is at best a poor substrate for small molecule pumps in the cell.
Two separate forward genetics screens in C.
elegans isolated seven independent psymberin-resistant mutants. In each the mutation was a C361T point mutation in the rpl-41 gene that changes Pro65 to Leu65 in the protein coding sequence. The psymberin-resistant mutant strain DA2312 is resistant to psymberin only. This mutation did not appear to cause weaker binding of psymberin to the ribosome, but must allow translation to continue with the toxin bound.
There are additional modes of actions of psymberin compared to mycalamide A. The endogenous protein level of LC3, an autophagy marker, is decreased faster with psymberin treatment than mycalamide A. In HT-29 cells, psymberin is capable of synergizing TNFa-induced necrotic cell death more efficiently than mycalamide A. The results from SAR study and from study of the psymberin-specific mutation in C.
elegans suggest that psymberin may induce fast cell death through multiple pathways, including translation inhibition, apoptosis and necrosis. The structural uniqueness of psymberin has functional consequences suggesting that the mode of action of psymberin on the ribosome is different from other members of the pederin family.
Advisors/Committee Members: Roth, Michael G..
Subjects/Keywords: Pyrones; Caenorhabditis elegans Proteins; Cell Death
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APA (6th Edition):
Wu, C. (2011). Using C. Elegans as Model Organism to Study the Mode of Action of a Natural Toxin, Psymberin. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/956
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):
Wu, Cheng-Yang. “Using C. Elegans as Model Organism to Study the Mode of Action of a Natural Toxin, Psymberin.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021.
http://hdl.handle.net/2152.5/956.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Wu, Cheng-Yang. “Using C. Elegans as Model Organism to Study the Mode of Action of a Natural Toxin, Psymberin.” 2011. Web. 07 Mar 2021.
Vancouver:
Wu C. Using C. Elegans as Model Organism to Study the Mode of Action of a Natural Toxin, Psymberin. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2152.5/956.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Wu C. Using C. Elegans as Model Organism to Study the Mode of Action of a Natural Toxin, Psymberin. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/956
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Texas Southwestern Medical Center
29.
Potts, Malia Beth.
Genetic Analysis of Hox Transcription Factors and Cofactors in the Regulation of Programmed Cell Death in C Elegans.
Degree: 2009, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/685
► It has been well established that blocking apoptosis can promote cancer. Throughout the animal kingdom, apoptosis is exquisitely regulated in cell-specific and context-specific ways to…
(more)
▼ It has been well established that blocking apoptosis can promote cancer. Throughout the animal kingdom, apoptosis is exquisitely regulated in cell-specific and context-specific ways to ensure proper development and tissue homeostasis. In many cases, transcriptional pathways carry out this regulation by mechanisms that are not completely understood. Studies of programmed cell death in the nematode
Caenorhabditis elegans provided an essential foundation for understanding the more complex pathways of apoptosis in mammals. More recent work, including my thesis research, has focused on the mechanisms that decide whether individual cells of C.
elegans survive or undergo programmed cell death, and has revealed a striking concordance of transcription factors that regulate cell death and that cause cancer in humans when altered by mutation. These findings suggest that mutations affecting these transcriptional pathways can provide a survival advantage to cancer cells, and thus may represent promising novel therapeutic targets.
Advisors/Committee Members: Cameron, Scott.
Subjects/Keywords: Apoptosis; Caenorhabditis elegans
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APA (6th Edition):
Potts, M. B. (2009). Genetic Analysis of Hox Transcription Factors and Cofactors in the Regulation of Programmed Cell Death in C Elegans. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/685
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):
Potts, Malia Beth. “Genetic Analysis of Hox Transcription Factors and Cofactors in the Regulation of Programmed Cell Death in C Elegans.” 2009. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021.
http://hdl.handle.net/2152.5/685.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Potts, Malia Beth. “Genetic Analysis of Hox Transcription Factors and Cofactors in the Regulation of Programmed Cell Death in C Elegans.” 2009. Web. 07 Mar 2021.
Vancouver:
Potts MB. Genetic Analysis of Hox Transcription Factors and Cofactors in the Regulation of Programmed Cell Death in C Elegans. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2009. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2152.5/685.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Potts MB. Genetic Analysis of Hox Transcription Factors and Cofactors in the Regulation of Programmed Cell Death in C Elegans. [Thesis]. University of Texas Southwestern Medical Center; 2009. Available from: http://hdl.handle.net/2152.5/685
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
East Carolina University
30.
Lish, Luke R.
Effects of Zinc Oxide Nanoparticles on the Pharyngeal Pumping and Neurological Behavior of C. elegans.
Degree: MS, MS-Molecular Biology & Biotech, 2018, East Carolina University
URL: http://hdl.handle.net/10342/6911
► Cogent data regarding the effects of manufactured zinc oxide nanoparticles (ZnO-NPs) on human health and other organisms is limited. With the prominence of manufactured ZnO…
(more)
▼ Cogent data regarding the effects of manufactured zinc oxide nanoparticles (ZnO-NPs) on human health and other organisms is limited. With the prominence of manufactured ZnO - NPs increasing rapidly in recent years, the identification of prolonged consequences of exposure to the NPs is crucial. Thus, further study regarding their biological effects is highly significant. The purpose of this research is to discern the potential toxicological effects of manufactured zinc oxide nanoparticles (0.614, 61.4, and 614 [micro]M Zn corresponding to 0.05, 5, and 50 [micro]g/L ZnO) on the pharyngeal pumping and neurological behaviors of the nematode
Caenorhabditis elegans (C.
elegans). While several studies have examined endpoints regarding behavior, reproduction efficacy, lethality and transgene expression after exposure to ZnO - NPs, insufficient attention has been allocated to the effects of the ZnO - NPs on the "heart" of the nematode, the pharynx. This experiment is designed to test hypotheses that exposure to ZnO - NPs results in aberrant neurological behavior and alternations in the pharyngeal pumping of C.
elegans. Behavioral assays have been performed on C.
elegans exposed to three different concentrations of manufactured ZnO - NPs (0.614, 61.4, and 614 [micro]M Zn) for different exposure times. Results suggest that C.
elegans at different developmental stages respond to ZnO NPs exposure differently, and different exposure durations also result in different behavioral responses. Exposure of L4 C.
elegans to ZnO-NPs at 61.4 and 614 [micro]M for 1 hour significantly reduced pharyngeal pumping and body bends. Adult 3-day-old C.
elegans exposed to ZnO-NPs at 0.614, 61.4 and 614 [micro]M for 24 hours displayed significantly increased pharyngeal pumping as compared to the control. The enhanced pumping rate on 3-day-old adult worms followed a temporal pattern and lasted until at least 72 hours of ZnO NP treatment for the 61.4 [micro]M group. Whereas for the 4-day-old C.
elegans, treatment with ZnO 0.614, 61.4 and 614 [micro]M for relatively short periods of time (1 hr and 4 hrs) do not have significant effects on pharyngeal pumping as compared to control, while prolonged treatment to 24 hours significantly decreased pharyngeal pumping, head thrashes, and body bends. A total of 23 genes that are related to pharyngeal pumping and stress response were selected to test their expressions on 3-day-old C.
elegans treated with ZnO NPs at 61.4 [micro]M for 72 hours: ceh-22, ceh-24, daf-12, drp-1, dyn-1, eat-2, eat-5, eat-18, F02A9.4, glc-2, inx-10, lev-11, myo-1, myo-2, myo-5, nas-3, nas-15, nfi-1, pha-1, pha-2, pha-4, sod-1 and unc-2. Overall, a majority of the said genes, 17 out of 23, were significantly upregulated. Genes that exhibited significant > 2 fold upregulation include ceh-22, daf-12, drp-1, dyn-1, eat-5, eat-18, F02A9.4, glc-2, myo-1, myo-5, nas-3, nas-15, nfi-1, pha-1, pha-2, sod-1 and unc-2. Only three genes were downregulated: ceh-24, myo-2 and pha-4. Since the number of conserved genes from C.
elegans to humans is…
Advisors/Committee Members: Pan, Xiaoping (committee member).
Subjects/Keywords: nanoparticles; Caenorhabditis elegans; Zinc oxide – Toxicity testing
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APA (6th Edition):
Lish, L. R. (2018). Effects of Zinc Oxide Nanoparticles on the Pharyngeal Pumping and Neurological Behavior of C. elegans. (Masters Thesis). East Carolina University. Retrieved from http://hdl.handle.net/10342/6911
Chicago Manual of Style (16th Edition):
Lish, Luke R. “Effects of Zinc Oxide Nanoparticles on the Pharyngeal Pumping and Neurological Behavior of C. elegans.” 2018. Masters Thesis, East Carolina University. Accessed March 07, 2021.
http://hdl.handle.net/10342/6911.
MLA Handbook (7th Edition):
Lish, Luke R. “Effects of Zinc Oxide Nanoparticles on the Pharyngeal Pumping and Neurological Behavior of C. elegans.” 2018. Web. 07 Mar 2021.
Vancouver:
Lish LR. Effects of Zinc Oxide Nanoparticles on the Pharyngeal Pumping and Neurological Behavior of C. elegans. [Internet] [Masters thesis]. East Carolina University; 2018. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10342/6911.
Council of Science Editors:
Lish LR. Effects of Zinc Oxide Nanoparticles on the Pharyngeal Pumping and Neurological Behavior of C. elegans. [Masters Thesis]. East Carolina University; 2018. Available from: http://hdl.handle.net/10342/6911
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