subject:(neural crest )

University of Southern California

1. Das, Ankita. Tissue interactions & molecular pathways in specification of the ectomesenchyme from cranial neural crest.

Degree: PhD, Genetic, Molecular and Cellular Biology, 2012, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/40333/rec/7494

► Vertebrate cranial neural crest cells (CNCCs) contribute not only to ectodermal lineages like neurons, glia and pigment but also to “ectomesenchymal” lineages like cartilage and… (more)

Subjects/Keywords: ectomesenchyme; neural crest

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APA (6^th Edition):

Das, A. (2012). Tissue interactions & molecular pathways in specification of the ectomesenchyme from cranial neural crest. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/40333/rec/7494

Chicago Manual of Style (16^th Edition):

Das, Ankita. “Tissue interactions & molecular pathways in specification of the ectomesenchyme from cranial neural crest.” 2012. Doctoral Dissertation, University of Southern California. Accessed March 04, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/40333/rec/7494.

MLA Handbook (7^th Edition):

Das, Ankita. “Tissue interactions & molecular pathways in specification of the ectomesenchyme from cranial neural crest.” 2012. Web. 04 Mar 2021.

Vancouver:

Das A. Tissue interactions & molecular pathways in specification of the ectomesenchyme from cranial neural crest. [Internet] [Doctoral dissertation]. University of Southern California; 2012. [cited 2021 Mar 04]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/40333/rec/7494.

Council of Science Editors:

Das A. Tissue interactions & molecular pathways in specification of the ectomesenchyme from cranial neural crest. [Doctoral Dissertation]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/40333/rec/7494

Dalhousie University

2. Edsall, Sara C. Does Exposure to Simulated Microgravity Affect Cranial Neural Crest-Derived Tissues in Danio rerio?.

Degree: MS, Department of Anatomy & Neurobiology, 2011, Dalhousie University

URL: http://hdl.handle.net/10222/14238

► To determine whether exposure to simulated microgravity (SMG) affects cranial neural crest (CNC)-derived tissues, zebrafish embryos were exposed to SMG starting at one of three… (more)

Subjects/Keywords: zebrafish; microgravity; bone; neural crest; pigment; mesoderm

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APA (6^th Edition):

Edsall, S. C. (2011). Does Exposure to Simulated Microgravity Affect Cranial Neural Crest-Derived Tissues in Danio rerio?. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/14238

Chicago Manual of Style (16^th Edition):

Edsall, Sara C. “Does Exposure to Simulated Microgravity Affect Cranial Neural Crest-Derived Tissues in Danio rerio?.” 2011. Masters Thesis, Dalhousie University. Accessed March 04, 2021. http://hdl.handle.net/10222/14238.

MLA Handbook (7^th Edition):

Edsall, Sara C. “Does Exposure to Simulated Microgravity Affect Cranial Neural Crest-Derived Tissues in Danio rerio?.” 2011. Web. 04 Mar 2021.

Vancouver:

Edsall SC. Does Exposure to Simulated Microgravity Affect Cranial Neural Crest-Derived Tissues in Danio rerio?. [Internet] [Masters thesis]. Dalhousie University; 2011. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10222/14238.

Council of Science Editors:

Edsall SC. Does Exposure to Simulated Microgravity Affect Cranial Neural Crest-Derived Tissues in Danio rerio?. [Masters Thesis]. Dalhousie University; 2011. Available from: http://hdl.handle.net/10222/14238

University of Otago

3. Capon, Samuel James. Characterising Cfm2, a Novel Gene Involved in Vertebrate Development .

Degree: 2011, University of Otago

URL: http://hdl.handle.net/10523/2044

► The Cfm2 gene is conserved in vertebrates and is linked to various developmental anomalies in humans. This gene is a paralogue of another novel gene… (more)

▼ The Cfm2 gene is conserved in vertebrates and is linked to various developmental anomalies in humans. This gene is a paralogue of another novel gene named Cfm, for caudal forebrain and midbrain. In the mouse, Cfm was found to be expressed in the neuroectoderm, which forms the future caudal forebrain and midbrain, and also in the optic rudiment, first pharyngeal arch, Rathke’s pouch, tongue muscle, lung, inner wall of the alimentary canal, genital tubercle and peripheral nerves (Hirano et al., 2005). Also in the mouse, Cfm2 was found to be expressed in the presomitic mesoderm of the segmenting somite, the optic nerve, otic capsule, peripheral nerves, tegmentum, lung and tongue muscle (Hirano et al., 2005). More recently a yeast-two-hybrid screen found that FAM101A, the human orthologue of the CFM2 protein, binds to filamin A (FLNA) (Gay et al., 2011). Most instances of the otopalatodigital (OPD) syndrome spectrum of disorders are associated with mutations in FLNA, the gene encoding FLNA, however in some instances no such mutations are found (Robertson, 2007). This has led to a hypothesis implicating CFM2, the protein product of the Cfm2 gene, in the OPD syndrome spectrum of disorders through its interactions with FLNA. In silico analysis of the CFM and CFM2 proteins revealed this family to be very highly conserved in vertebrates with orthologues found in a number of vertebrate Classes. Orthologues were also identified in the lancelet, a primitive chordate with an ancestral relationship to the vertebrates. Phylogenetic analysis of these orthologues found the CFM and CFM2 proteins to form two distinct clades in the resulting tree, representing the CFM and CFM2 sequences respectively. These results strongly support the notion of the CFM and CFM2 sequences having arisen from a duplication event in a common ancestor of the Chordates. Reverse transcription PCR (RT-PCR) found that the Cfm gene is expressed continuously in Xenopus laevis development, and similarly in the development of the limb in Xenopus. In situ hybridisation found this expression to be located to the lateral plate mesoderm, neural tube floor plate, hypochord and the developing proctodeum at stage 30. Cfm expression was detected in the epidermal layer of the hindlimb during limb development. RT-PCR found that Cfm2 expression is much more restricted during development. In situ hybridisation found Cfm2 expression to be localised in the developing olfactory organ, lateral line precursors, pronephros and the branchial arches at stage 40 in Xenopus development. In the limbs, in situ hybridisation revealed Cfm2 to be expressed at the joints of the bones of the limb, in a manner consistent with the sequential formation of these structures. No overlapping expression was found between these genes, consistent with the notion of independent evolution in these two genes after the aforementioned duplication event. Down-regulation of Cfm2 using a morpholino oligonucleotide (MO) had diverse effects on Xenopus development. Cfm2 MO injected tadpoles developed at… Advisors/Committee Members: Beck, Caroline (advisor).

Subjects/Keywords: Cfm2; RefilinA; Fam101A; Xenopus; Neural crest; Filamin

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APA (6^th Edition):

Capon, S. J. (2011). Characterising Cfm2, a Novel Gene Involved in Vertebrate Development . (Masters Thesis). University of Otago. Retrieved from http://hdl.handle.net/10523/2044

Chicago Manual of Style (16^th Edition):

Capon, Samuel James. “Characterising Cfm2, a Novel Gene Involved in Vertebrate Development .” 2011. Masters Thesis, University of Otago. Accessed March 04, 2021. http://hdl.handle.net/10523/2044.

MLA Handbook (7^th Edition):

Capon, Samuel James. “Characterising Cfm2, a Novel Gene Involved in Vertebrate Development .” 2011. Web. 04 Mar 2021.

Vancouver:

Capon SJ. Characterising Cfm2, a Novel Gene Involved in Vertebrate Development . [Internet] [Masters thesis]. University of Otago; 2011. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10523/2044.

Council of Science Editors:

Capon SJ. Characterising Cfm2, a Novel Gene Involved in Vertebrate Development . [Masters Thesis]. University of Otago; 2011. Available from: http://hdl.handle.net/10523/2044

University of Bath

4. Gesell, Anne E. Investigating the role of Yes-associated protein (YAP) in neural crest development.

Degree: PhD, 2015, University of Bath

URL: https://researchportal.bath.ac.uk/en/studentthesis/investigating-the-role-of-yesassociated-protein-yap-in-neural-crest-development(7252d3e4-3730-4ab5-97eb-882d808973a5).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.681035

► The neural crest (NC) is a multipotent embryonic cell type derived from the ectoderm during neurulation giving rise to a variety of cell lineages such… (more)

▼ The neural crest (NC) is a multipotent embryonic cell type derived from the ectoderm during neurulation giving rise to a variety of cell lineages such as neurons, glia and pigment cells. Most genes associated with the correct initiation, differentiation and migration of the neural crest have been found through reverse genetics. Similarities between neural crest development and some features of cancer progression are remarkable. For instance, it has been suggested that some cancer types recapitulate NC processes in an unregulated manner such as epithelial-mesenchymal transition or active cell migration throughout the body to form distant metastases. However, to date very little is known about initiators and drivers that direct neural crest cell migration to specific target sites. The Medaka mutant hirame represents an interesting melanocyte specific migration defect on the yolk sac caused by a loss of functional Yes-associated protein (YAP). Medaka hirame mutants were initially studied for their profound changes in body morphology. Genomic mapping identified the causal mutation as a nonsense point mutation within the first WW domain in the Yes-associated protein 1 (YAP1), causing translation of a dysfunctional YAP protein. YAP is a downstream transcriptional co-activator of the recently discovered and evolutionarily conserved Hippo pathway. Alterations within Hippo signalling are linked to cell survival, proliferation and abnormal tissue overgrowth. We demonstrate that hirame melanocyte precursors (melanoblasts) are initially present in normal abundance, but show an early migration defect with a lack of melanoblasts on the yolk sac, and corresponding accumulation in the lateral parts of the body. Subsequently, we observe an overall decline in differentiated melanocyte numbers during late stage embryogenesis. We designed an overexpression cassette linking enhanced GFP to either wild type or a mutated activated version of YAP and present evidence that it can efficiently rescue the melanocyte defect after injection of mRNA into one-cell stage embryos. Furthermore, analysis of the yolk sac anatomy via transmission electron microscopy indicates that a fraction of yolk membrane cells undergo apoptosis and we propose that this may contribute to the establishment of altered environmental cues leading to abnormal melanoblast migration onto the yolk sac. Injection of yap mRNA directly into the yolk sac however, failed to rescue melanoblast patterning. To advance our study, we isolated and characterised a 3.6 kb Medaka dopachrome tautomerase (Dct) promoter fragment, and used it to drive expression of enhanced green fluorescent protein (eGFP) in vivo. We generated germline transgenics with this construct that showed lineage-specific expression of eGFP within early migrating melanoblasts, a phenotype that is maintained in differentiated melanocytes throughout embryogenesis. In addition, using this promoter we overexpressed our egfp-yap fusion cassette and established transgenic lines to assess the cell autonomy of YAP within the…

Subjects/Keywords: 612.8; neural crest, YAP, Medaka, Melanocytes

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APA (6^th Edition):

Gesell, A. E. (2015). Investigating the role of Yes-associated protein (YAP) in neural crest development. (Doctoral Dissertation). University of Bath. Retrieved from https://researchportal.bath.ac.uk/en/studentthesis/investigating-the-role-of-yesassociated-protein-yap-in-neural-crest-development(7252d3e4-3730-4ab5-97eb-882d808973a5).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.681035

Chicago Manual of Style (16^th Edition):

Gesell, Anne E. “Investigating the role of Yes-associated protein (YAP) in neural crest development.” 2015. Doctoral Dissertation, University of Bath. Accessed March 04, 2021. https://researchportal.bath.ac.uk/en/studentthesis/investigating-the-role-of-yesassociated-protein-yap-in-neural-crest-development(7252d3e4-3730-4ab5-97eb-882d808973a5).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.681035.

MLA Handbook (7^th Edition):

Gesell, Anne E. “Investigating the role of Yes-associated protein (YAP) in neural crest development.” 2015. Web. 04 Mar 2021.

Vancouver:

Gesell AE. Investigating the role of Yes-associated protein (YAP) in neural crest development. [Internet] [Doctoral dissertation]. University of Bath; 2015. [cited 2021 Mar 04]. Available from: https://researchportal.bath.ac.uk/en/studentthesis/investigating-the-role-of-yesassociated-protein-yap-in-neural-crest-development(7252d3e4-3730-4ab5-97eb-882d808973a5).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.681035.

Council of Science Editors:

Gesell AE. Investigating the role of Yes-associated protein (YAP) in neural crest development. [Doctoral Dissertation]. University of Bath; 2015. Available from: https://researchportal.bath.ac.uk/en/studentthesis/investigating-the-role-of-yesassociated-protein-yap-in-neural-crest-development(7252d3e4-3730-4ab5-97eb-882d808973a5).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.681035

5. LEE TECK HO, RAYMOND. ONTOGENESIS OF MURINE NEURAL CREST DERIVATIVES.

Degree: 2011, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/34493

Subjects/Keywords: Neural Crest; Ectomesenchyme

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APA (6^th Edition):

LEE TECK HO, R. (2011). ONTOGENESIS OF MURINE NEURAL CREST DERIVATIVES. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/34493

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

LEE TECK HO, RAYMOND. “ONTOGENESIS OF MURINE NEURAL CREST DERIVATIVES.” 2011. Thesis, National University of Singapore. Accessed March 04, 2021. http://scholarbank.nus.edu.sg/handle/10635/34493.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

LEE TECK HO, RAYMOND. “ONTOGENESIS OF MURINE NEURAL CREST DERIVATIVES.” 2011. Web. 04 Mar 2021.

Vancouver:

LEE TECK HO R. ONTOGENESIS OF MURINE NEURAL CREST DERIVATIVES. [Internet] [Thesis]. National University of Singapore; 2011. [cited 2021 Mar 04]. Available from: http://scholarbank.nus.edu.sg/handle/10635/34493.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

LEE TECK HO R. ONTOGENESIS OF MURINE NEURAL CREST DERIVATIVES. [Thesis]. National University of Singapore; 2011. Available from: http://scholarbank.nus.edu.sg/handle/10635/34493

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Arizona

6. Brummett, Elaine S., 1942-. Determination of chromatophores in amphibian neural crest explants .

Degree: 1967, University of Arizona

URL: http://hdl.handle.net/10150/318643

Subjects/Keywords: Chromatophores.; Neural crest.

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APA (6^th Edition):

Brummett, Elaine S., 1. (1967). Determination of chromatophores in amphibian neural crest explants . (Masters Thesis). University of Arizona. Retrieved from http://hdl.handle.net/10150/318643

Chicago Manual of Style (16^th Edition):

Brummett, Elaine S., 1942-. “Determination of chromatophores in amphibian neural crest explants .” 1967. Masters Thesis, University of Arizona. Accessed March 04, 2021. http://hdl.handle.net/10150/318643.

MLA Handbook (7^th Edition):

Brummett, Elaine S., 1942-. “Determination of chromatophores in amphibian neural crest explants .” 1967. Web. 04 Mar 2021.

Vancouver:

Brummett, Elaine S. 1. Determination of chromatophores in amphibian neural crest explants . [Internet] [Masters thesis]. University of Arizona; 1967. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10150/318643.

Council of Science Editors:

Brummett, Elaine S. 1. Determination of chromatophores in amphibian neural crest explants . [Masters Thesis]. University of Arizona; 1967. Available from: http://hdl.handle.net/10150/318643

University of Southern California

7. Schafer, Christopher A. The temporal and tissue specific requirement of Msx genes in murine skull vault osteogenesis.

Degree: PhD, Genetic, Molecular and Cellular Biology, 2011, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/636188/rec/7353

► The homeobox genes Msx1 and Msx2 are set of transcription factors known to have both widespread and overlapping expression patterns throughout the developing murine embryo.… (more)

▼ The homeobox genes Msx1 and Msx2 are set of transcription factors known to have both widespread and overlapping expression patterns throughout the developing murine embryo. Conventional inactivation of either or both of these genes has been associated with a variety of congenital abnormalities including defects in calvarial osteogenesis, palate formation, cardiac development, and embryonic lethality. Here we utilize conditional and temporal gene inactivation to investigate the role of these genes in the development of the murine skull vault. ❧ Temporal inactivation of Msx2 revealed a window of requirement for cranial osteogenesis. Concerted loss of both Msx1 and Msx2 showed an unexpected ability of neural crest derived tissues to contribute to the formation of ectopic bone. Along with this we demonstrated a more extended requirement for the basic helix-loop-helix transcription factor, Twist1, which when mutated causes multiple cranial malformations including craniosynostosis. Although conditional inactivation of Msx1 and Msx2 in neural crest or mesoderm derived tissue did manifest deficient frontal and parietal bone development respectively, only mesodermal inactivation resulted in premature coronal suture fusion. However, conditional targeting of Msx1 and Msx2 using either neural crest or mesoderm driven cre recombinase illustrated phenotypes in adjacent calvarial tissues. Consistent with the view that Msx1 and Msx2 are required for specific tissue-tissue interactions in vertebrate development, here I show that these genes act upstream of BMP4 in cranial mesoderm to initiate and maintain osteogenesis in both the parietal and posterior frontal bone regions. Together my data suggest (1) that Msx1, Msx2, and Twist1 have a crucial window of requirement in the formation of the murine skull vault, (2) that mesoderm derived Msx1 and Msx2 function upstream of the morphogen BMP4 to influence posterior frontal bone osteogenesis, (3) that mesoderm derived Msx1 and Msx2 establish and maintain non-osteogenic coronal suture mesenchyme. Advisors/Committee Members: Maxson, Robert E. (Committee Chair), Chai, Yang (Committee Member), Dubeau, Louis (Committee Member).

Subjects/Keywords: skull vault; neural crest; mesoderm; tamoxifen

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APA (6^th Edition):

Schafer, C. A. (2011). The temporal and tissue specific requirement of Msx genes in murine skull vault osteogenesis. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/636188/rec/7353

Chicago Manual of Style (16^th Edition):

Schafer, Christopher A. “The temporal and tissue specific requirement of Msx genes in murine skull vault osteogenesis.” 2011. Doctoral Dissertation, University of Southern California. Accessed March 04, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/636188/rec/7353.

MLA Handbook (7^th Edition):

Schafer, Christopher A. “The temporal and tissue specific requirement of Msx genes in murine skull vault osteogenesis.” 2011. Web. 04 Mar 2021.

Vancouver:

Schafer CA. The temporal and tissue specific requirement of Msx genes in murine skull vault osteogenesis. [Internet] [Doctoral dissertation]. University of Southern California; 2011. [cited 2021 Mar 04]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/636188/rec/7353.

Council of Science Editors:

Schafer CA. The temporal and tissue specific requirement of Msx genes in murine skull vault osteogenesis. [Doctoral Dissertation]. University of Southern California; 2011. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/636188/rec/7353

Montana Tech

8. Foltz, Lauren Elizabeth. CELL SIGNALING PATHWAYS IN CONTROL OF NEUROBLASTOMA AND HUMAN NEURAL CREST DEVELOPMENT.

Degree: PhD, 2019, Montana Tech

URL: https://scholarworks.umt.edu/etd/11443

► Receptor Tyrosine Kinases (RTKs) are a family of cell surface receptors that bind extracellular ligands and initiate cellular signaling pathways. These pathways ultimately influence… (more)

▼ Receptor Tyrosine Kinases (RTKs) are a family of cell surface receptors that bind extracellular ligands and initiate cellular signaling pathways. These pathways ultimately influence cellular behaviors such as cell proliferation, migration, and differentiation. Consequently, mutations and amplifications of RTK genes contribute to the development of several cancers, including neuroblastoma. Neuroblastoma originates from neural crest cells, which are formed as the neural tube closes during vertebrate development. The neural crest differentiates and migrates to form cells of several lineages including the peripheral nervous system, melanocytes, and craniofacial cartilage. These processes are tightly controlled by RTK signaling, and failures in differentiation may lead to uncontrolled cell growth and tumor formation. While extensive research has characterized individual RTK signaling pathways in control of neural crest differentiation, it is unknown how signals from several different receptors are integrated to produce a cellular response. In Chapter 2, we investigate the regulation of RTK activity through endocytosis, which controls RTK degradation and receptor recycling to the plasma membrane. Here we show that the SRC family kinases (SFKs) are located in endosomes of neuroblastoma cells, and are activated by RTKs. Furthermore, SFK localization within different endosome populations changed in response to signaling by ALK and KIT. The scaffold protein, PAG1, forms signaling complexes containing SFKs as well as members of other pathways downstream of RTKs. To understand how PAG1 directs pSFK endocytosis and sequestration, we generated a PAG1 protein lacking the transmembrane domain. We define a model where PAG1 directs pSFK localization in responses tailored to different receptors and overall signaling. PAG1 mutation increased SFK activity in cells, but decreased SFK activity in endosomes and reduced cell differentiation. In Chapter 3, to better understand differences in signaling between human neural crest and neuroblastoma, we generated neural crest stem cells from human embryonic stem cells. During differentiation, neural crest cells unexpectedly formed cartilage, a cell lineage derived from neural crest. We investigated the differentiation of craniofacial cartilage and developed a protocol for production of cartilage organoids. Organoids are a promising model for neural crest development as well as a potential source of cartilage for facial reconstructions.

Subjects/Keywords: cell signaling; craniofacial cartilage; neural crest; neuroblastoma

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APA (6^th Edition):

Foltz, L. E. (2019). CELL SIGNALING PATHWAYS IN CONTROL OF NEUROBLASTOMA AND HUMAN NEURAL CREST DEVELOPMENT. (Doctoral Dissertation). Montana Tech. Retrieved from https://scholarworks.umt.edu/etd/11443

Chicago Manual of Style (16^th Edition):

Foltz, Lauren Elizabeth. “CELL SIGNALING PATHWAYS IN CONTROL OF NEUROBLASTOMA AND HUMAN NEURAL CREST DEVELOPMENT.” 2019. Doctoral Dissertation, Montana Tech. Accessed March 04, 2021. https://scholarworks.umt.edu/etd/11443.

MLA Handbook (7^th Edition):

Foltz, Lauren Elizabeth. “CELL SIGNALING PATHWAYS IN CONTROL OF NEUROBLASTOMA AND HUMAN NEURAL CREST DEVELOPMENT.” 2019. Web. 04 Mar 2021.

Vancouver:

Foltz LE. CELL SIGNALING PATHWAYS IN CONTROL OF NEUROBLASTOMA AND HUMAN NEURAL CREST DEVELOPMENT. [Internet] [Doctoral dissertation]. Montana Tech; 2019. [cited 2021 Mar 04]. Available from: https://scholarworks.umt.edu/etd/11443.

Council of Science Editors:

Foltz LE. CELL SIGNALING PATHWAYS IN CONTROL OF NEUROBLASTOMA AND HUMAN NEURAL CREST DEVELOPMENT. [Doctoral Dissertation]. Montana Tech; 2019. Available from: https://scholarworks.umt.edu/etd/11443

University of Oklahoma

9. Yuan, Tian. INSIGHTS FROM LAMPREY INTO DEVELOPMENT AND EVOLUTION OF GLIA AND CRANIAL SENSORY GANGLIA.

Degree: PhD, 2018, University of Oklahoma

URL: http://hdl.handle.net/11244/299814

► During evolution, animal nervous systems have become increasingly complex. This complexity is based on the cumulative diversity of neural cells and the emergence of new… (more)

▼ During evolution, animal nervous systems have become increasingly complex. This complexity is based on the cumulative diversity of neural cells and the emergence of new nervous system structures. Among animals, vertebrates possess the most complex and specialized nervous system, which has evolved to contain diversified neural cell types that control organs with specialized functions. For the study of nervous system evolution, one outstanding question is how those novel cell types originated in the vertebrates. To address this question, this dissertation focuses on: 1) The evolution of one specific glial cell type in the vertebrate central nervous system (CNS)—oligodendrocytes, which form the myelin sheath in jawed vertebrate CNS; 2) The emergence of paired cranial sensory ganglia in the peripheral nervous system. Myelin is a membrane protein that enables specialized cells to form an insulating layer around axons to speed up conduction along nerve cells. This protein and the cell types that form it (oligodendrocytes in the CNS and Schwann cells in PNS) are thought to be novel in jawed vertebrates. However, how these cell types evolved remains unclear. We asked whether the emergence of oligodendrocytes could only have occurred after the genetic “toolkit” required for this cell type appeared, or instead if the required genetic regulatory mechanism predates the evolution of the oligodendrocyte cell type itself. To address this question, I chose the basal jawless vertebrate—sea lamprey, since jawless vertebrates diverged from the jawed vertebrates prior to the evolution of oligodendrocytes. We used gene expression analyses coupled with functional perturbation using CRISPR/Cas9 mediated genome editing of sea lamprey embryos. My results indicate that the core genetic mechanism required for oligodendrocyte development is present in this jawless vertebrate, even though they lack this cell type, suggesting a core network regulating gliogenesis arose in the last common vertebrate ancestor. Sea lampreys appear to use this ancestral regulatory mechanism to control development of motor root glia. After the divergence of jawless and jawed vertebrates, other genes including myelinating proteins, were recruited onto this ancestral genetic scaffold and triggered the evolution of oligodendrocytes. Next, I focused on the evolution of cranial ganglia in the peripheral nervous system (PNS) of vertebrates. Among jawed vertebrates, the sensory neurons present in cranial ganglia are derived from two different cell populations—neurogenic placodes and neural crest. However, likely mechanisms directing development of cranial ganglia in the vertebrate common ancestor remain unclear. To study the evolution of vertebrate cranial sensory ganglia, I determined functional cellular contributions to cranial ganglia development in lamprey. I used gene expression analysis, cell lineage tracing and genome editing functional analysis, to show that lamprey cranial sensory neurons are likely purely derived from placodes, while neural crest surround… Advisors/Committee Members: McCauley, David (advisor), Durica, David (committee member), Markham, Michael (committee member), Masly, John P (committee member), Schroeder, Susan (committee member).

Subjects/Keywords: oligodendrocytes; cranial ganglia; placode; neural crest

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APA (6^th Edition):

Yuan, T. (2018). INSIGHTS FROM LAMPREY INTO DEVELOPMENT AND EVOLUTION OF GLIA AND CRANIAL SENSORY GANGLIA. (Doctoral Dissertation). University of Oklahoma. Retrieved from http://hdl.handle.net/11244/299814

Chicago Manual of Style (16^th Edition):

Yuan, Tian. “INSIGHTS FROM LAMPREY INTO DEVELOPMENT AND EVOLUTION OF GLIA AND CRANIAL SENSORY GANGLIA.” 2018. Doctoral Dissertation, University of Oklahoma. Accessed March 04, 2021. http://hdl.handle.net/11244/299814.

MLA Handbook (7^th Edition):

Yuan, Tian. “INSIGHTS FROM LAMPREY INTO DEVELOPMENT AND EVOLUTION OF GLIA AND CRANIAL SENSORY GANGLIA.” 2018. Web. 04 Mar 2021.

Vancouver:

Yuan T. INSIGHTS FROM LAMPREY INTO DEVELOPMENT AND EVOLUTION OF GLIA AND CRANIAL SENSORY GANGLIA. [Internet] [Doctoral dissertation]. University of Oklahoma; 2018. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11244/299814.

Council of Science Editors:

Yuan T. INSIGHTS FROM LAMPREY INTO DEVELOPMENT AND EVOLUTION OF GLIA AND CRANIAL SENSORY GANGLIA. [Doctoral Dissertation]. University of Oklahoma; 2018. Available from: http://hdl.handle.net/11244/299814

10. Myers, Logan G. Origins of Ret Signaling in Development of the Insect Gut Nervous System: A Model for Enteric Nervous System Development.

Degree: 2017, University of Nevada – Reno

URL: http://hdl.handle.net/11714/2045

► Understanding the evolutionary origins of neurotrophic signaling guiding the formation and upkeep of the central and peripheral nervous systems (CNS/PNS), can offer insights into the… (more)

▼ Understanding the evolutionary origins of neurotrophic signaling guiding the formation and upkeep of the central and peripheral nervous systems (CNS/PNS), can offer insights into the basis of development and congenital diseases affecting those systems. In humans, fatal disorders caused by disturbed formation of the enteric nervous system (ENS) of the gut such as Hirschsprung’s disease as well as degeneration of dopamine neuron populations in Parkinson’s disease are multigenic. In short, these diseases have a confounding collection of genetic causes. Many years of research have provided scientists with numerous targets for treatment, however it is difficult to find new and investigate proposed genetic interactions due to research limitations of genetic studies. It is necessary to refine systems allowing genes and their products, involved in nervous system development, to be studied more easily and efficiently. Uncovering ancestral genes within families of trophic factors may also be key to finding novel targets to treat or stop the progression of these diseases.Development of the ENS in vertebrates, often referred to as the “second brain”, relies heavily on signaling from the Ret receptor tyrosine kinase (RTK). Mutations in Ret and/or its coreceptor and GDNF ligand lead to a condition characterized by lack of neural innervation in terminal portions of the gastrointestinal tract and loss of normal gut function in affected areas. Instances of this condition where mutations within genes of the Ret signaling complex cannot be identified leave investigators with questions about the genetic profile of the problem. Laboratories have established mouse and zebrafish models to study ENS development, but limitations arise in the degree to which the underlying genetics can be manipulated for study. It is important to have a system that can be used for genetic screens as well as system-based treatment studies that the current models cannot provide. This dissertation will describe such a system.The invertebrate fruit fly Drosophila melanogaster is a genetically accessible model system being used for studies of CNS and PNS development. Novel discoveries have been made in the fly regarding the cellular and molecular mechanisms guiding brain formation. Drosophila have a compact gut nervous system that we can use to study mechanisms guiding ENS formation. We have organized a genetic toolkit to study this system and examined the role that the fly Ret homolog has on the formation of its enteric neurons. We have found that loss of Ret signaling in the fly leads to defects in fly gut nervous system development and an equivalent condition to that seen in vertebrate models. Defects in embryonic enteric neurons lead to aberrant architecture of larval gut neurons. These flaws subsequently cause feeding defects and increased larval mortality. Additionally, we have evidence for the other members of the Ret signaling complex in the fly. This work shows that the protein Maverick functions as a proto-GDNF in invertebrates via a Gfrl co-receptor.… Advisors/Committee Members: Kidd, Thomas (advisor), Miura, Pedro (committee member), Renden, Robert (committee member), Zhang, Yong (committee member), Ward, Sean (committee member).

Subjects/Keywords: Drosophila; Enteric; Hirschsprungs; Neural crest; Ret; Stomatogastric

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Myers, L. G. (2017). Origins of Ret Signaling in Development of the Insect Gut Nervous System: A Model for Enteric Nervous System Development. (Thesis). University of Nevada – Reno. Retrieved from http://hdl.handle.net/11714/2045

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Myers, Logan G. “Origins of Ret Signaling in Development of the Insect Gut Nervous System: A Model for Enteric Nervous System Development.” 2017. Thesis, University of Nevada – Reno. Accessed March 04, 2021. http://hdl.handle.net/11714/2045.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Myers, Logan G. “Origins of Ret Signaling in Development of the Insect Gut Nervous System: A Model for Enteric Nervous System Development.” 2017. Web. 04 Mar 2021.

Vancouver:

Myers LG. Origins of Ret Signaling in Development of the Insect Gut Nervous System: A Model for Enteric Nervous System Development. [Internet] [Thesis]. University of Nevada – Reno; 2017. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11714/2045.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Myers LG. Origins of Ret Signaling in Development of the Insect Gut Nervous System: A Model for Enteric Nervous System Development. [Thesis]. University of Nevada – Reno; 2017. Available from: http://hdl.handle.net/11714/2045

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Helsinki

11. Päivinen Linda. Foxg1 null allele mice exhibit frontal bone developmental abnormalities.

Degree: Medicinska fakulteten, 2018, University of Helsinki

URL: http://hdl.handle.net/10138/236222

►

Forkhead box G1 proteiini (FOXG1) on transkriptiorepressori, joka osallistuu moniin eri signaalireitteihin. Se on aiemmalta nimeltään Brain Factor 1 (BF1) ja on tunnettu vaikutuksistaan neurogeneesiin.… (more)

▼

Forkhead box G1 proteiini (FOXG1) on transkriptiorepressori, joka osallistuu moniin eri signaalireitteihin. Se on aiemmalta nimeltään Brain Factor 1 (BF1) ja on tunnettu vaikutuksistaan neurogeneesiin. FOXG1 expressoituu esiaivoissa ja kasvojen alueen hermostopienan soluissa. Tutkimuksen tavoitteena oli tutkia FOXG1:n osuutta otsaluiden kehityksessä hiirillä. Tämä toteutettiin Foxg1- mutatoidun hiirilinjalla avulla, jossa Foxg1-alleeli korvattiin Cre-rekombinaasilla. Tutkimuksessa käytettiin geenitekniikan menetelmiä ja luuston analyysejä. Ero mutantti alkioiden Foxg1cre/cre ja villityypin alkioiden Foxg1+/+ välillä löytyi. Foxg1cre/cre mutanttialkioiden otsaluiden ja nenäluiden alueelta löytyi poikkeavuuksia. Otsaluiden välinen sauma oli tähden mallinen ja otsaluut olivat kapeampia, sekä kallot olivat pienempiä Foxg1cre/cre mutanttialkioilla. Epämuodostumien syytä etsittiin solujen erilaistumisesta ja sitä analysoitiin EDU-värjäyksillä. EDU-värjäykset suoritettiin kallon kehitykselle tärkeissä alkion kehityksen vaiheissa, mutta erilaistumisessa ei havaittu eroja. Foxg1-mRNA:n ekpressoitumista havaittiin esiaivoissa, mutta ei kehittyvän otsaluun mesenkyymissä. Tämä voi olla merkki siitä, että fenotyyppi voi johtua poikkeavuuksista esiaivojen – ja kallon mesenkyymin kudosinteraktiossa tai jo aiemman vaiheen poikkeavuudesta hermostopienan soluissa. Foxg1cre/cre mutantien ja Foxg1+/+ villityyppien välillä nähtiin poikkeavuuksia HNK1-hermostopienamarkkerin jakaumassa alkioissa iältään 9.5-12.5 päivää. Erot saattavat omalta osaltaan selittää kallon ja kasvojen alueen fenotyyppiä Foxg1cre/cre hiirillä. Hermostopienan vaelluksessa saattaa olla eroa Foxg1cre/cre ja villityypin Foxg1+/+ välillä.

Forkhead box G1 protein (FOXG1) is a transcription repressor that participates in multiple signaling pathways. FOXG1 formerly known as Brain factor 1 (BF1) is known for its effects on neurogenesis. FOXG1 is also expressed in the neural crest cells (NCC’s), specifically in the facial NCC’s that form the craniofacial structures. The aim of this study was to investigate the role of FOXG1 in the craniofacial bone development in mice and this was conducted by using a mouse strain with the Foxg1-gene targeted by Cre-recombinase (Cre), which represents Foxg1 null allele. Using a combination of mouse genetics, gene expression analysis and skeletal analysis was used and a difference was seen between mutated Foxg1cre/cre-embryos (MT) and wild type Foxg1+/+-embryos (WT). Abnormalities were found in the frontal region of the skull and in the nasal bones of the Foxg1cre/cre-embryos. The frontal suture was seen to be star shaped and wider in the mutants and the suture persisted after the WT suture narrowed. The frontal bones and the nasal bones were narrower, and the skulls were smaller in the MT – embryos compared to WT littermates. To analyze whether alteration in cell proliferation could account for these malformations, EDU-stainings at key stages of calvarial development were performed, but no abnormalities were found. Foxg1-mRNA was…

Subjects/Keywords: FoxG1; BF1; neural crest cells; mus musculus; FoxG1; BF1; neural crest cells; mus musculus

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Linda, P. (2018). Foxg1 null allele mice exhibit frontal bone developmental abnormalities. (Masters Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/10138/236222

Chicago Manual of Style (16^th Edition):

Linda, Päivinen. “Foxg1 null allele mice exhibit frontal bone developmental abnormalities.” 2018. Masters Thesis, University of Helsinki. Accessed March 04, 2021. http://hdl.handle.net/10138/236222.

MLA Handbook (7^th Edition):

Linda, Päivinen. “Foxg1 null allele mice exhibit frontal bone developmental abnormalities.” 2018. Web. 04 Mar 2021.

Vancouver:

Linda P. Foxg1 null allele mice exhibit frontal bone developmental abnormalities. [Internet] [Masters thesis]. University of Helsinki; 2018. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10138/236222.

Council of Science Editors:

Linda P. Foxg1 null allele mice exhibit frontal bone developmental abnormalities. [Masters Thesis]. University of Helsinki; 2018. Available from: http://hdl.handle.net/10138/236222

University of Minnesota

12. Lund, Caroline E. Differentiation and patterning of cells originating in the zebrafish neuroectoderm.

Degree: MS, Integrated Biosciences, 2013, University of Minnesota

URL: http://purl.umn.edu/156912

►

University of Minnesota M.S. thesis. May 2013. Major: Integrated Biosciences. Advisor: Dr. Jennifer O. Liang. 1 computer file (PDF); vi, 99 pages.

Vertebrate nervous system… (more)

▼

University of Minnesota M.S. thesis. May 2013. Major: Integrated Biosciences. Advisor: Dr. Jennifer O. Liang. 1 computer file (PDF); vi, 99 pages.

Vertebrate nervous system development requires a complex series of events to transform a flat neuroepithelium into complex structures containing specialized cell types. The anterior neuroectoderm gives rise to the brain and is the origin for some of the first neurons that differentiate. It is also the origin of the cranial neural crest cells that form craniofacial features. This thesis focuses on the embryonic development of two tissues that arise from the zebrafish anterior neuroectoderm, the epithalamus, a region of the dorsal forebrain, and the mandible, the lower jaw. Early in development, the flat neural plate folds into a neural tube. The pineal gland, an organ involved with circadian rhythms, begins as two precursor domains at the lateral edges of the neural plate that converge into a single tissue when the neural tube closes. The pineal gland, along with the parapineal gland and habenula nuclei, form the epithalamus in the dorsal forebrain. In embryos with open neural tubes, the left and the right sides of the pineal and surrounding epithalamus are widely spaced. I found that despite this displacement, pineal cell types differentiate normally and initiate their rhythmic function. Conversely left-right asymmetry in the epithalamus was lost; both sides exhibited left-sided characteristics. Further, this loss of asymmetry in the epithalamus was correlated to severity in neural tube defects. Embryos with left isomerism had significantly wider pineal anlage domains than those with normal or reversed asymmetry. Cranial neural crest cells from the dorsal neural tube migrate to form craniofacial structures, including the cartilaginous precursor to the mandible, Meckel's cartilage. The bigtime (bti) mutant exhibits reductions in mandibular development. I found that although cranial neural crest cells localize normally to the lower jaw region in these mutants, they fail to differentiate into functional chondrocytes that secrete a sufficient amount of collagenous extracellular matrix.

Advisors/Committee Members: Dr. Jennifer O. Liang.

Subjects/Keywords: Differentiation; Neural crest; Neural tube; Nodal signaling; Patterning; Pineal gland

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lund, C. E. (2013). Differentiation and patterning of cells originating in the zebrafish neuroectoderm. (Masters Thesis). University of Minnesota. Retrieved from http://purl.umn.edu/156912

Chicago Manual of Style (16^th Edition):

Lund, Caroline E. “Differentiation and patterning of cells originating in the zebrafish neuroectoderm.” 2013. Masters Thesis, University of Minnesota. Accessed March 04, 2021. http://purl.umn.edu/156912.

MLA Handbook (7^th Edition):

Lund, Caroline E. “Differentiation and patterning of cells originating in the zebrafish neuroectoderm.” 2013. Web. 04 Mar 2021.

Vancouver:

Lund CE. Differentiation and patterning of cells originating in the zebrafish neuroectoderm. [Internet] [Masters thesis]. University of Minnesota; 2013. [cited 2021 Mar 04]. Available from: http://purl.umn.edu/156912.

Council of Science Editors:

Lund CE. Differentiation and patterning of cells originating in the zebrafish neuroectoderm. [Masters Thesis]. University of Minnesota; 2013. Available from: http://purl.umn.edu/156912

University of Oxford

13. Elms, Paul. The role of the Zic genes in mouse neural crest development.

Degree: PhD, 2004, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:89d42621-6028-469f-a630-298ece9980ff ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414086

► The neural crest is an embryonic population of migratory, multipotent cells that are formed at the boundary of the neural and non-neural ectoderm around the… (more)

Subjects/Keywords: 573.863871935335; Neural crest; Neural development

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Elms, P. (2004). The role of the Zic genes in mouse neural crest development. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:89d42621-6028-469f-a630-298ece9980ff ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414086

Chicago Manual of Style (16^th Edition):

Elms, Paul. “The role of the Zic genes in mouse neural crest development.” 2004. Doctoral Dissertation, University of Oxford. Accessed March 04, 2021. http://ora.ox.ac.uk/objects/uuid:89d42621-6028-469f-a630-298ece9980ff ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414086.

MLA Handbook (7^th Edition):

Elms, Paul. “The role of the Zic genes in mouse neural crest development.” 2004. Web. 04 Mar 2021.

Vancouver:

Elms P. The role of the Zic genes in mouse neural crest development. [Internet] [Doctoral dissertation]. University of Oxford; 2004. [cited 2021 Mar 04]. Available from: http://ora.ox.ac.uk/objects/uuid:89d42621-6028-469f-a630-298ece9980ff ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414086.

Council of Science Editors:

Elms P. The role of the Zic genes in mouse neural crest development. [Doctoral Dissertation]. University of Oxford; 2004. Available from: http://ora.ox.ac.uk/objects/uuid:89d42621-6028-469f-a630-298ece9980ff ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414086

University of Minnesota

14. Lund, Caroline E. Differentiation and patterning of cells originating in the zebrafish neuroectoderm.

Degree: MS, Integrated Biosciences, 2013, University of Minnesota

URL: http://purl.umn.edu/156912

► Vertebrate nervous system development requires a complex series of events to transform a flat neuroepithelium into complex structures containing specialized cell types. The anterior neuroectoderm… (more)

▼ Vertebrate nervous system development requires a complex series of events to transform a flat neuroepithelium into complex structures containing specialized cell types. The anterior neuroectoderm gives rise to the brain and is the origin for some of the first neurons that differentiate. It is also the origin of the cranial neural crest cells that form craniofacial features. This thesis focuses on the embryonic development of two tissues that arise from the zebrafish anterior neuroectoderm, the epithalamus, a region of the dorsal forebrain, and the mandible, the lower jaw. Early in development, the flat neural plate folds into a neural tube. The pineal gland, an organ involved with circadian rhythms, begins as two precursor domains at the lateral edges of the neural plate that converge into a single tissue when the neural tube closes. The pineal gland, along with the parapineal gland and habenula nuclei, form the epithalamus in the dorsal forebrain. In embryos with open neural tubes, the left and the right sides of the pineal and surrounding epithalamus are widely spaced. I found that despite this displacement, pineal cell types differentiate normally and initiate their rhythmic function. Conversely left-right asymmetry in the epithalamus was lost; both sides exhibited left-sided characteristics. Further, this loss of asymmetry in the epithalamus was correlated to severity in neural tube defects. Embryos with left isomerism had significantly wider pineal anlage domains than those with normal or reversed asymmetry. Cranial neural crest cells from the dorsal neural tube migrate to form craniofacial structures, including the cartilaginous precursor to the mandible, Meckel's cartilage. The bigtime (bti) mutant exhibits reductions in mandibular development. I found that although cranial neural crest cells localize normally to the lower jaw region in these mutants, they fail to differentiate into functional chondrocytes that secrete a sufficient amount of collagenous extracellular matrix.

Subjects/Keywords: Differentiation; Neural crest; Neural tube; Nodal signaling; Patterning; Pineal gland

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lund, C. E. (2013). Differentiation and patterning of cells originating in the zebrafish neuroectoderm. (Masters Thesis). University of Minnesota. Retrieved from http://purl.umn.edu/156912

Chicago Manual of Style (16^th Edition):

Lund, Caroline E. “Differentiation and patterning of cells originating in the zebrafish neuroectoderm.” 2013. Masters Thesis, University of Minnesota. Accessed March 04, 2021. http://purl.umn.edu/156912.

MLA Handbook (7^th Edition):

Lund, Caroline E. “Differentiation and patterning of cells originating in the zebrafish neuroectoderm.” 2013. Web. 04 Mar 2021.

Vancouver:

Lund CE. Differentiation and patterning of cells originating in the zebrafish neuroectoderm. [Internet] [Masters thesis]. University of Minnesota; 2013. [cited 2021 Mar 04]. Available from: http://purl.umn.edu/156912.

Council of Science Editors:

Lund CE. Differentiation and patterning of cells originating in the zebrafish neuroectoderm. [Masters Thesis]. University of Minnesota; 2013. Available from: http://purl.umn.edu/156912

University of Otago

15. Holman, Sarah Katherine Fay. The Genetics of Skeletogenesis .

Degree: 2012, University of Otago

URL: http://hdl.handle.net/10523/2504

► WTX is a member of a protein family bearing no homology to proteins with known functional domains with in silico analysis, but is of substantial… (more)

▼ WTX is a member of a protein family bearing no homology to proteins with known functional domains with in silico analysis, but is of substantial interest because germline and somatic mutations lead to the developmental disease osteopathia striata congenita with cranial sclerosis and the childhood renal malignancy, Wilms tumour. The full-length spliceform, WTXS1 contains binding domains for ß-catenin, axin, axin2, WT1, APC, axin, p53, KEAP1, ß-TrCP2 and a domain that binds PIP2 that localises the protein to the plasma membrane. The alternatively spliced transcript, WTXS2, excludes residues that are represented in WTXS1 that mediate the binding of PIP2. These binding domains for multiple proteins facilitate the role of WTX in many cellular functions including the canonical WNT signalling pathway, relocalisation of the subcellular distribution of APC, cell cycle regulation and transcriptional regulation. The aim of this study was to characterise the functions and mechanistic properties of WTX that relate to the generation of OSCS using a combination of genotype-phenotype analysis, investigation of the phenotype in wtx morphant zebrafish and mRNA rescue experiments utilising mutated WTX alleles. A comprehensive genotype-phenotype analysis in a cohort of individuals with OSCS resulted in the characterisation of two subsets of the male phenotype, a severe disorder with multiple structural and patterning malformations resulting from mutations in WTX located 5’ to the first APC binding domain, and a milder manifestation that has additional neuromuscular anomalies and results from mutations in WTX located more 3’. The identification of three affected individuals with nephroblastomatosis, a precursor toward Wilms tumour, indicates that mutations in WTX may predispose toward formation of precursor lesions however additional mutations are probably required for progression to tumourigenesis. Utilisation of the zebrafish as a model organism for the function of wtx during development resulted in the definition of a novel role for wtx in the specification of neural crest cells. Knockdown of Wtx using morpholino oligonucleotide technology resulted in reduced specification of and a decrease in number of neural crest cells entering the branchial arches resulting in malformed craniofacial cartilage, loss of the enteric nervous system and pigmentation abnormalities. The wtx morphant phenotype was then used as readout for phenotypic rescue following injection of mRNA encoding modified WTX alleles. From these experiments it was concluded that WTXS2 is not necessary for correct embryogenesis and alleles that result in a severe OSCS phenotype in males are non-functional. Site-directed mutagenesis of residues involved in localisation of WTXS1 to the plasma membrane results in a non-functional allele that is unable to rescue the wtx morphant phenotype, suggesting this ability is essential for its function. In aggregate these studies have facilitated the definition of the critical domains required for correct function of WTX during… Advisors/Committee Members: Robertson, Stephen (advisor).

Subjects/Keywords: osteopathia striata with cranial sclerosis; wtx; skeletal dysplasia; neural crest

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Holman, S. K. F. (2012). The Genetics of Skeletogenesis . (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/2504

Chicago Manual of Style (16^th Edition):

Holman, Sarah Katherine Fay. “The Genetics of Skeletogenesis .” 2012. Doctoral Dissertation, University of Otago. Accessed March 04, 2021. http://hdl.handle.net/10523/2504.

MLA Handbook (7^th Edition):

Holman, Sarah Katherine Fay. “The Genetics of Skeletogenesis .” 2012. Web. 04 Mar 2021.

Vancouver:

Holman SKF. The Genetics of Skeletogenesis . [Internet] [Doctoral dissertation]. University of Otago; 2012. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10523/2504.

Council of Science Editors:

Holman SKF. The Genetics of Skeletogenesis . [Doctoral Dissertation]. University of Otago; 2012. Available from: http://hdl.handle.net/10523/2504

UCLA

16. Cavanaugh, Ann. The Role of Cardiac Neural Crest Cells in Zebrafish Heart Development.

Degree: Molec, Cell, & Dev Biology, 2015, UCLA

URL: http://www.escholarship.org/uc/item/23v9299p

► Early stages of cardiac development are well conserved among vertebrates. However, later morphological development results in a more complicated 4 chambered heart in mammals, while… (more)

▼ Early stages of cardiac development are well conserved among vertebrates. However, later morphological development results in a more complicated 4 chambered heart in mammals, while fish retain a simple two chambered heart. The onset of these morphological changes coincide with contribution of cells to the heart from the second heart field (SHF). Interestingly, despite the great morphological differences in the structures derived from precursors in the SHF in mammals and zebrafish, the signals regulating SHF development are conserved. Cardiac neural crest cells (CNCCs), which also contribute to later stages of cardiac development are well studied in chick and mouse models, but very little is known about the role of CNCCs in zebrafish heart development. It is possible that as with the SHF the molecular mechanisms of CNCC development is conserved among all vertebrates. In this study I aim to better define the role of CNCCs in zebrafish and determine how well the role for CNCCs is conserved. I show that there are two waves of CNCCs which contribute to the heart in zebrafish. The first invades the developing heart tube between 24 hpf and 30 hpf and gives rise to CNC derived cardiomyocytes. CNCCs with a myocardial fate have an invasive morphology as they enter the heart, and disrupt local adhesion molecules in neighboring cells. The second wave of CNCCs migrates along aortic arch artery 6, onto the ventral aorta by 80 hpf, and ultimately invades the BA. I find that both populations of CNC derived cells persist to adulthood. These two populations are separated not only by developmental time, but also by their response to FGF signaling as they migrate to the heart. The first wave is independent of Tbx1, and FGF signaling, and the second wave relies on FGF signaling for migration to the ventral aorta and BA. Ablation of NC leads to a variety of cardiac defects including reduced heart rate, defects in myocardial maturation, development of the BA and aorta, and defects in SHF contribution to the heart, as well as a dramatic increase of bmp4 expression, and a reduction of tbx1 expression. Many of the cardiac phenotypes I observe in NC ablated embryos are similar to those reported in other species, making zebrafish an ideal model to study signaling which may be important for CNC development in vertebrates.

Subjects/Keywords: Developmental biology; Heart; Neural Crest; Second heart field; Zebrafish

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cavanaugh, A. (2015). The Role of Cardiac Neural Crest Cells in Zebrafish Heart Development. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/23v9299p

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Cavanaugh, Ann. “The Role of Cardiac Neural Crest Cells in Zebrafish Heart Development.” 2015. Thesis, UCLA. Accessed March 04, 2021. http://www.escholarship.org/uc/item/23v9299p.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Cavanaugh, Ann. “The Role of Cardiac Neural Crest Cells in Zebrafish Heart Development.” 2015. Web. 04 Mar 2021.

Vancouver:

Cavanaugh A. The Role of Cardiac Neural Crest Cells in Zebrafish Heart Development. [Internet] [Thesis]. UCLA; 2015. [cited 2021 Mar 04]. Available from: http://www.escholarship.org/uc/item/23v9299p.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Cavanaugh A. The Role of Cardiac Neural Crest Cells in Zebrafish Heart Development. [Thesis]. UCLA; 2015. Available from: http://www.escholarship.org/uc/item/23v9299p

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

17. Tiemey, Brent Jonathan. Effects of Homocysteine on Cardiac Neural Crest Cell Formation.

Degree: M.S. in Biomedical Sciences, Biomedical Sciences (graduate program), 2002, Creighton University

URL: http://hdl.handle.net/10504/68459

► Elevated homocysteine (Hcys) causes a wide spectrum of congenital detects, many of which resemble neural crest (NC) cell ablation. However, the etiological mechanism is not… (more)

▼ Elevated homocysteine (Hcys) causes a wide spectrum of congenital detects, many of which resemble neural crest (NC) cell ablation. However, the etiological mechanism is not known. The purpose of this study was to determine if Hcys altered the number and/or the proliferation of NC cells or their progenitors /?? Uw. Hcys was experimentally elevated in chicken embryos, 16 or 4 hrs before the stage when NC cells in the cardiac region of the neural tube began forming and migrating away from the neural tube. To evaluate the effect of Hcys on cell proliferation, 5-bromo-2'-deoxyuridine (BrdU) was used to label cells in S- phase of the cell cycle. In control embryos, a significantly higher percentage of newly formed NC cells were in S-phase compared to migrating NC cells or their progenitors within the neural tube. These results parallel those of other investigators showing in the trunk axial level, NC progenitor cells must enter the S-phase in order to segregate from the neural tube Elevated Hcys significantly decreased the number of NC cells but also increased neural tube cell number. Yet, the net total number of these cells was not different from control embryos. Hcys also decreased the BrdU-labeling index for newly formed NC cells These observations suggested Hcys inhibits NC progenitors from becoming NC ceils by blocking or delaying their entry into the S-phase. Hcys also decreased the distance NC cells migrated. Although Hcys-treated embryos had significantly fewer NC cells, there was a significant increase in the number of premigratory NC cells compared to controls. Premigratory NC cells in Hcys- treated embryos also had altered BrdU-labeling patterns and more mitotic figures than control embryos. This suggests Hcys also delayed the onset of N C cell migration once they became segregated from the neural tube. These results support the hypothesis that Hcys reduces the number of NC cells in the cardiac neural tube axial level by altering normal proliferation patterns of NC progenitor cells. It also provides the first in vivio evidence that NC morphogenesis is directly altered by elevated Hcys. Advisors/Committee Members: Brauer, Philip R. (advisor), Tiemey, Brent Jonathan (cuauthor).

Subjects/Keywords: Homocysteine; Neural Crest – cytology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tiemey, B. J. (2002). Effects of Homocysteine on Cardiac Neural Crest Cell Formation. (Masters Thesis). Creighton University. Retrieved from http://hdl.handle.net/10504/68459

Chicago Manual of Style (16^th Edition):

Tiemey, Brent Jonathan. “Effects of Homocysteine on Cardiac Neural Crest Cell Formation.” 2002. Masters Thesis, Creighton University. Accessed March 04, 2021. http://hdl.handle.net/10504/68459.

MLA Handbook (7^th Edition):

Tiemey, Brent Jonathan. “Effects of Homocysteine on Cardiac Neural Crest Cell Formation.” 2002. Web. 04 Mar 2021.

Vancouver:

Tiemey BJ. Effects of Homocysteine on Cardiac Neural Crest Cell Formation. [Internet] [Masters thesis]. Creighton University; 2002. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10504/68459.

Council of Science Editors:

Tiemey BJ. Effects of Homocysteine on Cardiac Neural Crest Cell Formation. [Masters Thesis]. Creighton University; 2002. Available from: http://hdl.handle.net/10504/68459

18. Cai, Dong Hong. Matrix Metalloproteinase Activity is an Important Mediator of Cardiac Neural Crest Cell Migration.

Degree: PhD, Biomedical Sciences (graduate program), 2001, Creighton University

URL: http://hdl.handle.net/10504/65336

► Matrix metalloproteinases (MMPs) are a family of zinc proteolytic enzymes important in embryonic development and pathological processes. Cardiac neural crest (CNC) cells are derived from… (more)

▼ Matrix metalloproteinases (MMPs) are a family of zinc proteolytic enzymes important in embryonic development and pathological processes. Cardiac neural crest (CNC) cells are derived from the dorsal portion of neural tube through an epithehal-to - mesenchymal cell transition and then migrate along the basement membrane of ectoderm, enter the pharyngeal arches, and subsequently participate in the septation of the heart during embryonic development. My studies showed that one of the MMPs, MMP-2 (gelatinase A, or 72 kDa type IV collagenase), was deposited in CNC migration pathway and was expressed by CNC cells after they entered the pharyngeal arches. Furthermore, the distribution pattern of MMP-2 was disrupted by migrating CNC cells. This suggested that MMP enzymatic activity might play an important role in CNC migration. To test this hypothesis, a synthetic MMP inhibitor KB8301 was injected into the cell-free space adjacent to the premigratory CNC cells. The distance that CNC migrated in the injected side was significantly decreased compared with that in the noninjected side and in the vehicle treated embryos. Enzyme activity assays showed that the activity of MMPs decreased about 30% after KB8301 injection. This demonstrated that enzymatic activity of MMPs is an important mediator for CNC migration. The natural inhibitors of MMPs, TIMPs, were also studied. TIMP-2, which not only has the inhibitory activity against MMPs, but also participates in the activation of proMMP-2, was expressed exclusively in a subpopulation of CNC cells during their early migration. Local delivery of exogenous TIMP-2 significantly decreased CNC migratory distance as well as MMP activity in vivo. The pattern of TIMP-3 expression suggests that this inhibitor is not likely to have a role in early NC migration but could be involved in pharyngeal arch and cardiac. Overall, my studies support the hypothesis that MMP activity is an important mediator of CNC cell migration. Advisors/Committee Members: Brauer, Philip R. (advisor), Cai, Dong Hong (cuauthor).

Subjects/Keywords: Heart – embryology; Neural Crest – embryology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cai, D. H. (2001). Matrix Metalloproteinase Activity is an Important Mediator of Cardiac Neural Crest Cell Migration. (Doctoral Dissertation). Creighton University. Retrieved from http://hdl.handle.net/10504/65336

Chicago Manual of Style (16^th Edition):

Cai, Dong Hong. “Matrix Metalloproteinase Activity is an Important Mediator of Cardiac Neural Crest Cell Migration.” 2001. Doctoral Dissertation, Creighton University. Accessed March 04, 2021. http://hdl.handle.net/10504/65336.

MLA Handbook (7^th Edition):

Cai, Dong Hong. “Matrix Metalloproteinase Activity is an Important Mediator of Cardiac Neural Crest Cell Migration.” 2001. Web. 04 Mar 2021.

Vancouver:

Cai DH. Matrix Metalloproteinase Activity is an Important Mediator of Cardiac Neural Crest Cell Migration. [Internet] [Doctoral dissertation]. Creighton University; 2001. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10504/65336.

Council of Science Editors:

Cai DH. Matrix Metalloproteinase Activity is an Important Mediator of Cardiac Neural Crest Cell Migration. [Doctoral Dissertation]. Creighton University; 2001. Available from: http://hdl.handle.net/10504/65336

19. Νικολοπούλου, Πηνελόπη. Μελέτη της έκφρασης γονιδίων που επηρεάζουν τον κυτταρικό κύκλο και τη μοίρα των βλαστικών κυττάρων της νευρικής ακρολοφίας σε έμβρυα μυός απουσία της πρωτεΐνης Geminin.

Degree: 2014, University of Patras

URL: http://hdl.handle.net/10889/8536

►

Τα κύτταρα της νευρικής ακρολοφίας (Neural Crest Cells - NCCs) αποτελούν έναν πολυδύναμο, μεταναστευτικό πληθυσμός βλαστικών κυττάρων τα οποία δίνουν γένεση σε μια πληθώρα κυτταρικών… (more)

▼

Τα κύτταρα της νευρικής ακρολοφίας (Neural Crest Cells - NCCs) αποτελούν έναν πολυδύναμο, μεταναστευτικό πληθυσμός βλαστικών κυττάρων τα οποία δίνουν γένεση σε μια πληθώρα κυτταρικών τύπων κατά την ανάπτυξη των σπονδυλωτών, συμπεριλαμβανομένων των νευρώνων και των νευρογλοιακών κυττάρων του περιφερικού νευρικού συστήματος (ΠΝΣ). Η δημιουργία των κυττάρων της νευρικής ακρολοφίας πραγματοποιείται στο στάδιο της γαστριδίωσης μετά την επαγωγή της νευρικής πλάκας. Οι διαδικασίες αυτές επηρεάζονται από σηματοδοτικά μονοπάτια στα οποία εμπλέκονται τόσο μεταγραφικοί παράγοντες όσο και επιγενετικοί τροποποιητές . Το Εντερικό Νευρικό Σύστημα (ΕΝΣ), προέρχεται από τα κύτταρα της νευρικής ακρολοφίας της αυχενικής και της ιερής μοίρας και ελέγχει την ομαλή λειτουργία της γαστρεντερικής οδού. Τα κύτταρα της νευρικής ακρολοφίας της αυχενικής μοίρας αποικίζουν ολόκληρο τον εντερικό σωλήνα και δίνουν γένεση στο ΕΝΣ ξεκινώντας από την 9η εμβρυική ημέρα. Η δημιουργία ενός πλήρως λειτουργικού ΕΝΣ εξαρτάται από την ικανότητα μετανάστευσης, πολλαπλασιασμού και διαφοροποίησης των NCCs. Στόχος της παρούσας διπλωματικής εργασίας ήταν η μελέτη της έκφρασης γονιδίων που ελέγχουν τον πολλαπλασιασμό και τη μετανάστευση τόσο των πρόδρομων κυττάρων της νευρικής ακρολοφίας όσο και των NCCs που έχουν δεσμευτεί προς εντερική μοίρα σε έμβρυα μυός απουσία της πρωτεΐνης Geminin. Η Geminin είναι μια πρωτεΐνη που έχει δειχθεί να επηρεάζει την ισορροπία μεταξύ αυτο-ανανέωσης και διαφοροποίησης, μέσω της αλληλεπίδρασης της με μεταγραφικούς παράγοντες και πρωτεΐνες αναδιαμόρφωσης της χρωματίνης. Με σκοπό να διερευνήσουμε τον in vivo ρόλο της Geminin στα κύτταρα της νευρικής ακρολοφίας, δημιουργήσαμε διαγονιδιακούς μύες από τους οποίους αδρανοποιήσαμε το γονίδιο της Geminin ειδικά στα κύτταρα της νευρικής ακρολοφίας. Τα αποτελέσματα μας έδειξαν ότι η απουσία της Geminin από τα κύτταρα της νευρικής ακρολοφίας, οδηγεί στη δημιουργία εμβρύων με μορφολογικές αλλοιώσεις κατά τα πρώιμα στάδια της ανάπτυξης ενώ σε μεταγενέστερα αναπτυξιακά στάδια χαρακτηρίζονται από σοβαρές κρανιοπροσωπικές δυσμορφίες. Επιπλέον, η ιστοειδική αδρανοποίηση της Geminin οδήγησε σε απορρύθμιση των επιπέδων έκφρασης γονιδίων που επηρεάζουν τόσο την επαγωγή όσο και τη μετανάστευση των NCCs (mChd7, mSnail2, mTwist2,mFoxD3) κατά την 10.5η εμβρυική ημέρα. Μελέτη του κυτταρικού κύκλου των εντερικών κυττάρων νευρικής ακρολοφίας έδειξε ότι η αποσιώπηση της Geminin διαταράσσει το προφίλ του κυτταρικού τους κύκλου καθώς τα κύτταρα αυτά «μπλοκάρουν» κατά τη μετάβαση από την G2 στη Μ φάση (E9.5). Συμπερασματικά, τα αποτελέσματά μας δείχνουν ότι η Geminin συμμετέχει ενεργά στον ρύθμιση της έκφρασης γονιδίων που παίζουν σημαντικό ρόλο στην επαγωγή και τη μετανάστευση των NCCs κατά τα πρώιμα στάδια της εμβρυικής ανάπτυξης (Ε10.5). Τέλος, η Geminin διαδραματίζει σημαντικό ρόλο στον πολλαπλασιασμό των πρόδρομων κυττάρων του εντερικού νευρικού συστήματος (Ε9.5).

Neural Crest cells (NCCs) comprise a multipotent, migratory cell population that generates a diverse array of cell and tissue types…

Advisors/Committee Members: Ταραβήρας, Σταύρος, Nikolopoulou, Pinelopi, Λυγερού, Ζωή, Μητσάκου, Αδαμαντία.

Subjects/Keywords: Κύτταρα νευρικής ακρολοφίας; 616.027 74; Neural crest cells; Geminin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Νικολοπούλου, �. (2014). Μελέτη της έκφρασης γονιδίων που επηρεάζουν τον κυτταρικό κύκλο και τη μοίρα των βλαστικών κυττάρων της νευρικής ακρολοφίας σε έμβρυα μυός απουσία της πρωτεΐνης Geminin. (Masters Thesis). University of Patras. Retrieved from http://hdl.handle.net/10889/8536

Chicago Manual of Style (16^th Edition):

Νικολοπούλου, Πηνελόπη. “Μελέτη της έκφρασης γονιδίων που επηρεάζουν τον κυτταρικό κύκλο και τη μοίρα των βλαστικών κυττάρων της νευρικής ακρολοφίας σε έμβρυα μυός απουσία της πρωτεΐνης Geminin.” 2014. Masters Thesis, University of Patras. Accessed March 04, 2021. http://hdl.handle.net/10889/8536.

MLA Handbook (7^th Edition):

Νικολοπούλου, Πηνελόπη. “Μελέτη της έκφρασης γονιδίων που επηρεάζουν τον κυτταρικό κύκλο και τη μοίρα των βλαστικών κυττάρων της νευρικής ακρολοφίας σε έμβρυα μυός απουσία της πρωτεΐνης Geminin.” 2014. Web. 04 Mar 2021.

Vancouver:

Νικολοπούλου �. Μελέτη της έκφρασης γονιδίων που επηρεάζουν τον κυτταρικό κύκλο και τη μοίρα των βλαστικών κυττάρων της νευρικής ακρολοφίας σε έμβρυα μυός απουσία της πρωτεΐνης Geminin. [Internet] [Masters thesis]. University of Patras; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10889/8536.

Council of Science Editors:

Νικολοπούλου �. Μελέτη της έκφρασης γονιδίων που επηρεάζουν τον κυτταρικό κύκλο και τη μοίρα των βλαστικών κυττάρων της νευρικής ακρολοφίας σε έμβρυα μυός απουσία της πρωτεΐνης Geminin. [Masters Thesis]. University of Patras; 2014. Available from: http://hdl.handle.net/10889/8536

University of Manchester

20. Losa Llabata, Marta. Gene regulation in embryonic development.

Degree: 2016, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:295949

► Branchial arches (BAs) are a series of transient structures that develop on the ventro-lateral surface of the head in vertebrate embryos. BAs initially appear as… (more)

▼ Branchial arches (BAs) are a series of transient structures that develop on the ventro-lateral surface of the head in vertebrate embryos. BAs initially appear as a series of similar segments; as development proceeds each BA will contribute to different structures. Here, it was investigated the transcriptional mechanisms that instruct the different fates of the BAs in development. Initially, each BA contains a blood vessel, known as aortic arch (AA) artery, that connects the dorsal aorta with the heart. Remodelling of the AAs is crucial to form the adult heart circulation. This process leads to regression of the anterior AAs, running though the first and second BAs (BA1 and BA2), and persistence of the AAs contained in more posterior BAs (PBA). To identify the mechanisms that control remodelling of the AAs, we compared the transcriptomes and epigenomic landscapes of different BAs. Using RNA-seq and H3K27Ac ChIP-seq, we uncovered the activation of a vascular smooth muscle cell (VSMC) differentiation transcriptional program exclusively in the PBAs (and not in BA1/BA2). In support of this finding, we show that VSMC differentiation occurs specifically in the PBAs, but not BA1-2 in mouse embryonic development. Despite the absence of VSMC differentiation in developing BA1-2, cells harvested from these tissues reveal a spontaneous tendency to differentiate towards VSMC fate when grown in vitro, and activate several VSMC-specific genes (Myocd, Acta2, Tagln, Jag1). Together, our results suggest that forming VSMCs is a key process for the persistence of AAs. We also showed that cells derived from all BAs have the potential to differentiate to VSMCs in vitro. However, only cells in the PBAs differentiate to VSMCs in vivo, resulting in the maintenance of posterior AAs. In this study, we also uncovered a novel transcriptional principle that specifies the fate of BA2. Using ChIP-seq, we found that binding of Meis transcription factors establish a ground pattern in the BAs. Hoxa2, which specifies BA2 identity, selects a subset of Meis-bound sites. Meis binding is strongly increased at these sites, which coincide with active enhancers, linked to genes highly expressed in the BA2 and regulated by Hoxa2. Thus, Hoxa2 modifies a ground state binding of Meis to instruct segment-specific transcriptional programs. Advisors/Committee Members: HENTGES, KATHRYN KE, Hentges, Kathryn, Bobola, Nicoletta.

Subjects/Keywords: branchial arch; neural crest cells; aortic arch; vascular smooth muscle cells

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Losa Llabata, M. (2016). Gene regulation in embryonic development. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:295949

Chicago Manual of Style (16^th Edition):

Losa Llabata, Marta. “Gene regulation in embryonic development.” 2016. Doctoral Dissertation, University of Manchester. Accessed March 04, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:295949.

MLA Handbook (7^th Edition):

Losa Llabata, Marta. “Gene regulation in embryonic development.” 2016. Web. 04 Mar 2021.

Vancouver:

Losa Llabata M. Gene regulation in embryonic development. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Mar 04]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:295949.

Council of Science Editors:

Losa Llabata M. Gene regulation in embryonic development. [Doctoral Dissertation]. University of Manchester; 2016. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:295949

Vanderbilt University

21. Ritter, Karen Elaine. Serotonin Signaling in the Neural Development and Function of the Lower Urinary Tract.

Degree: PhD, Neuroscience, 2018, Vanderbilt University

URL: http://hdl.handle.net/1803/10413

► The autonomic and sensory nervous systems are derived from the neural crest and are required for the normal functioning of visceral organ systems, including the… (more)

Subjects/Keywords: bladder; Htr3a; sensory nervous system; autonomic nervous system; neural crest; development

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ritter, K. E. (2018). Serotonin Signaling in the Neural Development and Function of the Lower Urinary Tract. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10413

Chicago Manual of Style (16^th Edition):

Ritter, Karen Elaine. “Serotonin Signaling in the Neural Development and Function of the Lower Urinary Tract.” 2018. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/10413.

MLA Handbook (7^th Edition):

Ritter, Karen Elaine. “Serotonin Signaling in the Neural Development and Function of the Lower Urinary Tract.” 2018. Web. 04 Mar 2021.

Vancouver:

Ritter KE. Serotonin Signaling in the Neural Development and Function of the Lower Urinary Tract. [Internet] [Doctoral dissertation]. Vanderbilt University; 2018. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/10413.

Council of Science Editors:

Ritter KE. Serotonin Signaling in the Neural Development and Function of the Lower Urinary Tract. [Doctoral Dissertation]. Vanderbilt University; 2018. Available from: http://hdl.handle.net/1803/10413

Vanderbilt University

22. Mundell, Nathan Andrew. Regulation of multipotency and self-renewal in neural crest stem cells: analysis of foxd3 function in diverse neural crest cell populations.

Degree: PhD, Pharmacology, 2011, Vanderbilt University

URL: http://hdl.handle.net/1803/11113

► During vertebrate development, neural crest (NC) cells migrate from the dorsal neural tube and generate a wide variety of cell types throughout the embryo including… (more)

▼ During vertebrate development, neural crest (NC) cells migrate from the dorsal neural tube and generate a wide variety of cell types throughout the embryo including neurons, glia, melanocytes, smooth muscle, cartilage and bone. The formation of NC progenitors has been extensively studied, yet molecules controlling NC multipotency and self-renewal and factors mediating cell-intrinsic distinctions between multipotent versus fate-restricted progenitors are poorly understood. As part of my thesis work, I show that the transcription factor Foxd3 mediates a fate restriction choice for multipotent NC progenitors with loss of Foxd3 biasing NC toward a mesenchymal fate. Neural derivatives of NC were lost in Foxd3 mutant mouse embryos, whereas abnormally-fated NC-derived vascular smooth muscle cells were ectopically located in the aorta. Cranial NC defects were associated with precocious differentiation towards osteoblast and chondrocyte cell fates, and individual mutant NC from different anterior-posterior regions underwent fate changes, losing neural and increasing myofibroblast potential. During development of the enteric nervous system (ENS) Foxd3 expression is maintained in NC progenitors and glia. Using a novel Ednrb-iCre transgene to delete Foxd3 after NC migrate into the midgut, I demonstrated a late temporal requirement for Foxd3 during ENS development. Fate mapping in Foxd3 mutant embryos revealed a reduction of ENS progenitors throughout the gut and loss of Ednrb-iCre lineage cells in the distal colon. Although mutant mice were viable, defects in ENS patterning were associated with severe reduction of glial cells derived from the Ednrb-iCre lineage. Lineage and differentiation analysis suggested a compensatory population of Foxd3-positive progenitors that did not express Ednrb-iCre in mutant embryos. My findings highlight the roles played by Foxd3 during ENS development including proliferation of ENS progenitors, neural patterning, and glial differentiation. Collectively, these data suggest Foxd3 functions as a critical regulator of NC fate potential and establish novel parallels between NC and other progenitor populations that depend on this functionally conserved stem cell protein to regulate multipotency and self-renewal. Advisors/Committee Members: Patricia A. Labosky (committee member), Kendal S. Broadie (committee member), Ronald B. Emeson (committee member), Michelle Southard-Smith (committee member), Joey V. Barnett (Committee Chair).

Subjects/Keywords: Stem cells; neural crest; Foxd3; transcription factor; multipotency; mouse development

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mundell, N. A. (2011). Regulation of multipotency and self-renewal in neural crest stem cells: analysis of foxd3 function in diverse neural crest cell populations. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11113

Chicago Manual of Style (16^th Edition):

Mundell, Nathan Andrew. “Regulation of multipotency and self-renewal in neural crest stem cells: analysis of foxd3 function in diverse neural crest cell populations.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/11113.

MLA Handbook (7^th Edition):

Mundell, Nathan Andrew. “Regulation of multipotency and self-renewal in neural crest stem cells: analysis of foxd3 function in diverse neural crest cell populations.” 2011. Web. 04 Mar 2021.

Vancouver:

Mundell NA. Regulation of multipotency and self-renewal in neural crest stem cells: analysis of foxd3 function in diverse neural crest cell populations. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/11113.

Council of Science Editors:

Mundell NA. Regulation of multipotency and self-renewal in neural crest stem cells: analysis of foxd3 function in diverse neural crest cell populations. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/11113

Vanderbilt University

23. Pfaltzgraff, Elise Rachel. Studies on the Cellular and Molecular Regulation of Cardiovascular Development.

Degree: PhD, Cell and Developmental Biology, 2014, Vanderbilt University

URL: http://hdl.handle.net/1803/12619

► A developing vertebrate embryo can only subsist for a finite time without a vasculature. The vascular system is one of the earliest organ systems to… (more)

Subjects/Keywords: developmental biology; cardiovascular development; microtubule dynamics; neural crest

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pfaltzgraff, E. R. (2014). Studies on the Cellular and Molecular Regulation of Cardiovascular Development. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/12619

Chicago Manual of Style (16^th Edition):

Pfaltzgraff, Elise Rachel. “Studies on the Cellular and Molecular Regulation of Cardiovascular Development.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/12619.

MLA Handbook (7^th Edition):

Pfaltzgraff, Elise Rachel. “Studies on the Cellular and Molecular Regulation of Cardiovascular Development.” 2014. Web. 04 Mar 2021.

Vancouver:

Pfaltzgraff ER. Studies on the Cellular and Molecular Regulation of Cardiovascular Development. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/12619.

Council of Science Editors:

Pfaltzgraff ER. Studies on the Cellular and Molecular Regulation of Cardiovascular Development. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/12619

Vanderbilt University

24. Musser, Melissa Anne. Enteric nervous system deficits in the ganglionated bowel of Hirschsprung mouse models and patients.

Degree: PhD, Human Genetics, 2014, Vanderbilt University

URL: http://hdl.handle.net/1803/14756

► Hirschsprung disease, or congenital absence of ganglia in the distal intestine, occurs in approximately every 1 in 5000 live births. Although HSCR patients have the… (more)

Subjects/Keywords: Hirschsprung; enteric nervous system; neural crest; Sox10; Ret; Ednrb

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APA (6^th Edition):

Musser, M. A. (2014). Enteric nervous system deficits in the ganglionated bowel of Hirschsprung mouse models and patients. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14756

Chicago Manual of Style (16^th Edition):

Musser, Melissa Anne. “Enteric nervous system deficits in the ganglionated bowel of Hirschsprung mouse models and patients.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/14756.

MLA Handbook (7^th Edition):

Musser, Melissa Anne. “Enteric nervous system deficits in the ganglionated bowel of Hirschsprung mouse models and patients.” 2014. Web. 04 Mar 2021.

Vancouver:

Musser MA. Enteric nervous system deficits in the ganglionated bowel of Hirschsprung mouse models and patients. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/14756.

Council of Science Editors:

Musser MA. Enteric nervous system deficits in the ganglionated bowel of Hirschsprung mouse models and patients. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14756

West Virginia University

25. Perfetto, Mark Stephen. Canonical Wnt Mechanisms in Neural Crest Induction.

Degree: PhD, Biology, 2019, West Virginia University

URL: https://doi.org/10.33915/etd.7393 ; https://researchrepository.wvu.edu/etd/7393

► Canonical Wnt signaling is a pathway that is critical for normal development and the progression of disease. The canonical Wnt signaling pathway was put… (more)

Subjects/Keywords: Canonical Wnt Signaling; ADAMs; Akt signaling; neural crest; Biology; Developmental Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Perfetto, M. S. (2019). Canonical Wnt Mechanisms in Neural Crest Induction. (Doctoral Dissertation). West Virginia University. Retrieved from https://doi.org/10.33915/etd.7393 ; https://researchrepository.wvu.edu/etd/7393

Chicago Manual of Style (16^th Edition):

Perfetto, Mark Stephen. “Canonical Wnt Mechanisms in Neural Crest Induction.” 2019. Doctoral Dissertation, West Virginia University. Accessed March 04, 2021. https://doi.org/10.33915/etd.7393 ; https://researchrepository.wvu.edu/etd/7393.

MLA Handbook (7^th Edition):

Perfetto, Mark Stephen. “Canonical Wnt Mechanisms in Neural Crest Induction.” 2019. Web. 04 Mar 2021.

Vancouver:

Perfetto MS. Canonical Wnt Mechanisms in Neural Crest Induction. [Internet] [Doctoral dissertation]. West Virginia University; 2019. [cited 2021 Mar 04]. Available from: https://doi.org/10.33915/etd.7393 ; https://researchrepository.wvu.edu/etd/7393.

Council of Science Editors:

Perfetto MS. Canonical Wnt Mechanisms in Neural Crest Induction. [Doctoral Dissertation]. West Virginia University; 2019. Available from: https://doi.org/10.33915/etd.7393 ; https://researchrepository.wvu.edu/etd/7393

Virginia Commonwealth University

26. Spencer, Samantha A. The Role of tfec in Zebrafish Neural Crest Cell and RPE Development.

Degree: MS, Human Genetics, 2015, Virginia Commonwealth University

URL: https://doi.org/10.25772/TYVZ-HB14 ; https://scholarscompass.vcu.edu/etd/3754

► Zebrafish (Danio rerio) show a unique pigmentation pattern comprised of three pigment cell types: melanophores, iridophores and xanthophores. Other pigmented cells include the retinal… (more)

Subjects/Keywords: RPE; neural crest; pigment; MITF; TFEC; Danio rerio; Genetics

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APA (6^th Edition):

Spencer, S. A. (2015). The Role of tfec in Zebrafish Neural Crest Cell and RPE Development. (Thesis). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/TYVZ-HB14 ; https://scholarscompass.vcu.edu/etd/3754

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Spencer, Samantha A. “The Role of tfec in Zebrafish Neural Crest Cell and RPE Development.” 2015. Thesis, Virginia Commonwealth University. Accessed March 04, 2021. https://doi.org/10.25772/TYVZ-HB14 ; https://scholarscompass.vcu.edu/etd/3754.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Spencer, Samantha A. “The Role of tfec in Zebrafish Neural Crest Cell and RPE Development.” 2015. Web. 04 Mar 2021.

Vancouver:

Spencer SA. The Role of tfec in Zebrafish Neural Crest Cell and RPE Development. [Internet] [Thesis]. Virginia Commonwealth University; 2015. [cited 2021 Mar 04]. Available from: https://doi.org/10.25772/TYVZ-HB14 ; https://scholarscompass.vcu.edu/etd/3754.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Spencer SA. The Role of tfec in Zebrafish Neural Crest Cell and RPE Development. [Thesis]. Virginia Commonwealth University; 2015. Available from: https://doi.org/10.25772/TYVZ-HB14 ; https://scholarscompass.vcu.edu/etd/3754

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas Medical Center

27. Bonilla-Claudio, Margarita. BMP-SIGNALING REGULATES A COMMON TRANSCRIPTIONAL PROGRAM TO CONTROL FACIAL FORM AND SKELETAL MORPHOGENESIS.

Degree: PhD, 2011, Texas Medical Center

URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/210

► Much of the craniofacial skeleton, such as the skull vault, mandible and midface, develops through direct, intramembranous ossification of the cranial neural crest (CNC)… (more)

Subjects/Keywords: Bone morphogenetic protein; morphogenesis; neural crest; Medicine and Health Sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bonilla-Claudio, M. (2011). BMP-SIGNALING REGULATES A COMMON TRANSCRIPTIONAL PROGRAM TO CONTROL FACIAL FORM AND SKELETAL MORPHOGENESIS. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/210

Chicago Manual of Style (16^th Edition):

Bonilla-Claudio, Margarita. “BMP-SIGNALING REGULATES A COMMON TRANSCRIPTIONAL PROGRAM TO CONTROL FACIAL FORM AND SKELETAL MORPHOGENESIS.” 2011. Doctoral Dissertation, Texas Medical Center. Accessed March 04, 2021. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/210.

MLA Handbook (7^th Edition):

Bonilla-Claudio, Margarita. “BMP-SIGNALING REGULATES A COMMON TRANSCRIPTIONAL PROGRAM TO CONTROL FACIAL FORM AND SKELETAL MORPHOGENESIS.” 2011. Web. 04 Mar 2021.

Vancouver:

Bonilla-Claudio M. BMP-SIGNALING REGULATES A COMMON TRANSCRIPTIONAL PROGRAM TO CONTROL FACIAL FORM AND SKELETAL MORPHOGENESIS. [Internet] [Doctoral dissertation]. Texas Medical Center; 2011. [cited 2021 Mar 04]. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/210.

Council of Science Editors:

Bonilla-Claudio M. BMP-SIGNALING REGULATES A COMMON TRANSCRIPTIONAL PROGRAM TO CONTROL FACIAL FORM AND SKELETAL MORPHOGENESIS. [Doctoral Dissertation]. Texas Medical Center; 2011. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/210

28. Σταθοπούλου, Αθανασία. Μελέτη του ρόλου του μορίου της geminin στον πολλαπλασιασμό, μετανάστευση και διαφοροποίηση πολυδύναμων κυττάρων της νευρικής ακρολοφίας σε γενετικά τροποποιημένους μύες.

Degree: 2012, University of Patras

URL: http://hdl.handle.net/10889/8831

► Τα κύτταρα της νευρικής ακρολοφίας είναι ένας πολυδύναμος πληθυσμός βλαστικών κυττάρων που δημιουργείται στη ραχιαία πλευρά του νευρικού σωλήνα των σπονδυλωτών κατά τη διάρκεια της… (more)

▼ Τα κύτταρα της νευρικής ακρολοφίας είναι ένας πολυδύναμος πληθυσμός βλαστικών κυττάρων που δημιουργείται στη ραχιαία πλευρά του νευρικού σωλήνα των σπονδυλωτών κατά τη διάρκεια της νευριδίωσης. Μετά τη δημιουργία τους, τα κύτταρα της νευρικής ακρολοφίας μεταναστεύουν σε ολόκληρο το έμβρυο, ακολουθώντας συγκεκριμένα μονοπάτια, συνεισφέροντας στη δημιουργία μιας μεγάλης ποικιλίας δομών, όπως νευρικά και γλοιακά κύτταρα του περιφερικού νευρικού συστήματος (ΠΝΣ), μελανοκύττρα, δομές που συμβάλλουν στο σκελετό του κρανίου και του προσώπου κλπ. Η δημιουργία, η αυτο- ανανέωση και η διαφοροποίηση των κυττάρων της νευρικής ακρολοφίας απαιτούν το συντονισμό των διεργασιών του κυτταρικού πολλαπλασιασμού και της κυτταρικής διαφοροποίησης. Η αδυναμία συντονισμού των παραπάνω διαδικασιών οδηγεί στην εμφάνιση ασθενειών στον άνθρωπο (neurocristopathies). Η Geminin είναι ένα μόριο που έχει την ικανότητα να ρυθμίζει την πρόοδο του κυτταρικού κύκλου, αλληλεπιδρώντας με τον παράγοντα αδειοδότησης της αντιγραφής Cdt1, και τη διαφοροποίηση, μέσω της αλληλεπίδρασής της με μεταγραφικούς παράγοντες και πρωτεΐνες αναδιαμόρφωσης της χρωματίνης. Προηγούμενες μελέτες του εργαστηρίου μας έχουν αναδείξει τη Geminin ως ένα σημαντικό ρυθμιστή των διαδικασιών της αυτο- ανανέωσης και διαφοροποίησης στα πρόδρομα νευρικά κύτταρα στον αναπτυσσόμενο φλοιό. Προκειμένου να κατανοήσουμε τους μηχανισμούς που ελέγχουν την αυτο-ανανέωση και τη διαφοροποίηση των πολυδύναμων κυττάρων της νευρικής ακρολοφίας και να κατανοήσουμε το μοριακό μηχανισμό ασθενειών στον άνθρωπο που σχετίζονται με την απορρύθμιση του ελέγχου της ι κανότητας αυτο-ανανέωσης και διαφοροποίησης των πολυδύναμων κυττάρων της νευρικής ακρολοφίας μελετήσαμε το ρόλο της Geminin στη δημιουργία, την αυτο-ανανέωση, τον καθορισμό και τη διαφοροποίηση των κυττάρων της νευρικής ακρολοφίας. Προς αυτή την κατεύθυνση πραγματοποιήθηκαν τόσο in vivo όσο και in vitro πειράματα, χρησιμοποιώντας ζωικά μοντέλα τα οποία δημιουργήθηκαν από το εργαστήριο μας και στα οποία το γονίδιο της Geminin είχε αδρανοποιηθεί ειδικά στα κύτταρα της νευρικής ακρολοφίας. Τα αποτελέσματά μας έδειξαν ότι η απουσία της Geminin οδηγεί στη δημιουργία εμβρύων με σοβαρές μορφολογικές αλλοιώσεις, που κατά τα πρώιμα αναπτυξιακά στάδια χαρακτηρίζονται από την απουσία της δομής του μεσεγκεφάλου και των βραγχιακών τόξων και σε μεταγενέστερα αναπτυξιακά στάδια εμφανίζουν σοβαρή κρανιοπροσωπική δυσμορφία, με κατάληξη το θάνατο των εμβρύων, λίγες ημέρες πριν γεννηθούν. Επιπλέον, κατά τα πρώιμα αναπτυξιακά στάδια παρατηρήθηκαν σοβαρές αλλοιώσεις σε δομές που προέρχονται από τη νευρική ακρολοφία, όπως είναι τα κρανιακά και τα ραχιαία γάγγλια, οι γναθικές προεκβολές και τα πρόδρομα κύτταρα του εντερικού νευρικού συστήματος. Η μείωση του πληθυσμού των πρόδρομων κυττάρων του εντερικού νευρικού συστήματος (ΕΝΣ) οδήγησε στη δημιουργία ενός αγαγγλιονικού εντέρου, το οποίο παρομοιάζει με το φαινότυπο του ΕΝΣ στη νόσο Hirschsprung στον άνθρωπο. Η ιστοειδική αδρανοποίηση της Geminin οδήγησε στη μείωση των… Advisors/Committee Members: Ταραβήρας, Σταύρος, Stathopoulou, Athanasia, Ταραβήρας, Σταύρος, Μητσάκου, Αδαμαντία, Πάχνης, Βασίλειος, Λυγερού, Ζωή, Πέτρου-Παπαδάκη, Ελένη, Νικολοπούλου, Βασιλική, Γιομπρές, Παναγιώτης.

Subjects/Keywords: Νευρική ακρολοφία; Εντερικό νευρικό σύστημα; 591.3; Neural crest; Enteric nervous system

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Σταθοπούλου, �. (2012). Μελέτη του ρόλου του μορίου της geminin στον πολλαπλασιασμό, μετανάστευση και διαφοροποίηση πολυδύναμων κυττάρων της νευρικής ακρολοφίας σε γενετικά τροποποιημένους μύες. (Doctoral Dissertation). University of Patras. Retrieved from http://hdl.handle.net/10889/8831

Chicago Manual of Style (16^th Edition):

Σταθοπούλου, Αθανασία. “Μελέτη του ρόλου του μορίου της geminin στον πολλαπλασιασμό, μετανάστευση και διαφοροποίηση πολυδύναμων κυττάρων της νευρικής ακρολοφίας σε γενετικά τροποποιημένους μύες.” 2012. Doctoral Dissertation, University of Patras. Accessed March 04, 2021. http://hdl.handle.net/10889/8831.

MLA Handbook (7^th Edition):

Σταθοπούλου, Αθανασία. “Μελέτη του ρόλου του μορίου της geminin στον πολλαπλασιασμό, μετανάστευση και διαφοροποίηση πολυδύναμων κυττάρων της νευρικής ακρολοφίας σε γενετικά τροποποιημένους μύες.” 2012. Web. 04 Mar 2021.

Vancouver:

Σταθοπούλου �. Μελέτη του ρόλου του μορίου της geminin στον πολλαπλασιασμό, μετανάστευση και διαφοροποίηση πολυδύναμων κυττάρων της νευρικής ακρολοφίας σε γενετικά τροποποιημένους μύες. [Internet] [Doctoral dissertation]. University of Patras; 2012. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10889/8831.

Council of Science Editors:

Σταθοπούλου �. Μελέτη του ρόλου του μορίου της geminin στον πολλαπλασιασμό, μετανάστευση και διαφοροποίηση πολυδύναμων κυττάρων της νευρικής ακρολοφίας σε γενετικά τροποποιημένους μύες. [Doctoral Dissertation]. University of Patras; 2012. Available from: http://hdl.handle.net/10889/8831

California State University – San Bernardino

29. Quiroz, Vincent. THE DEVELOPMENT OF AN H1 EMBRYONIC STEM CELL LINE TO STUDY THE ROLE OF THE ONCOGENES LMO1 AND MYCN IN HUMAN NEUROBLASTOMA FORMATION.

Degree: MSin Biology, Biology, 2020, California State University – San Bernardino

URL: https://scholarworks.lib.csusb.edu/etd/1125

► Neuroblastoma (NB) is an extracranial tumor that affects the nervous system and accounts for approximately 650 – 800 cases diagnosed per year in children… (more)

▼ Neuroblastoma (NB) is an extracranial tumor that affects the nervous system and accounts for approximately 650 – 800 cases diagnosed per year in children under the age of 5 (www.cancer.org/cancer/neuroblastoma/about/key-statistics.html). NB occurs at a relatively rare rate of 10.2 per million children under 15 years old but accounts for 12-15% of pediatric cancer death because patients with high-risk NB (HRNB) have 5-year survival rates between 40-50%(Brodeur, 2003; Park et al. 2010). Developmental biology research has recognized neural crest cells (NCC) as the progenitor cells of NB, as tumors form in the trunk NC derived sympathetic nervous system (Dupin, 2013; Simões-Costa et al., 2015). Genome-wide association studies (GWAS) of these tumors reveal several chromosomal aberrations and genes related to the development of NB (Pugh et al., 2013; Seeger et al., 1985). Unfortunately, the heterogeneity of the disease has revealed a low mutation frequency in suspected oncogenes, along with an assortment of chromosomal gains and losses, resulting in a variety of mechanisms of NB formation. These structural features demonstrate the complexity of NB tumorigenesis and the unlikeliness of developing a single target treatment (Matthay, K et al., 2012). Amongst all the predictors recognized in NB formation, amplification of the MYCN gene occurs in 20% of tumors and serves as the most significant prognosticator of poor outcomes in HRNB patients (Brodeur, 1984). These insights have resulted in NCC experiments in mice, zebrafish, and primary cell models to study NB development under the overexpression of MYCN and other oncogenes such as ALK and LMO1(Weiss et al.,1997; Zhu et al., 2012; Olsen et al., 2017). While these models have elucidated the association of MYCN and LMO1 overexpression in NCC to NB formation, they lack a direct descriptive model of NB formation in human NCC. Building off the current understanding of genes synergistically driving neuroblastoma, I utilized H1 human embryonic stem cells (hESC) to create a cell line inducible for LMO1 and MYCN. Through genetic engineering, and subcloning, I created two constructs: a plasmid containing the MYCN gene under the regulation of the Tetracycline On (TET-ON) system and the LMO1 construct under the regulation of TET-ON. I sequenced the constructs, analyzed their genetic composition, and found the TET-ON LMO1 suitable for integration into the H1 hESC. After nucleofection and genetic screening, the data suggest the production of a mixed population of H1 hESC containing a subset of cells that appear to have integrated the TET-ON LMO1 into the AAVS1 locus at chromosome 19. Further attempts are required for the complete development of the H1 hESC TET- 3G LMO1 plus MYCN inducible cell line. Advisors/Committee Members: Bournias-Vardiabasis, Nicole.

Subjects/Keywords: LMO1; MYCN; Neuroblastoma; Neural Crest Cells; H1 hESC; Biology; Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Quiroz, V. (2020). THE DEVELOPMENT OF AN H1 EMBRYONIC STEM CELL LINE TO STUDY THE ROLE OF THE ONCOGENES LMO1 AND MYCN IN HUMAN NEUROBLASTOMA FORMATION. (Thesis). California State University – San Bernardino. Retrieved from https://scholarworks.lib.csusb.edu/etd/1125

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Quiroz, Vincent. “THE DEVELOPMENT OF AN H1 EMBRYONIC STEM CELL LINE TO STUDY THE ROLE OF THE ONCOGENES LMO1 AND MYCN IN HUMAN NEUROBLASTOMA FORMATION.” 2020. Thesis, California State University – San Bernardino. Accessed March 04, 2021. https://scholarworks.lib.csusb.edu/etd/1125.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Quiroz, Vincent. “THE DEVELOPMENT OF AN H1 EMBRYONIC STEM CELL LINE TO STUDY THE ROLE OF THE ONCOGENES LMO1 AND MYCN IN HUMAN NEUROBLASTOMA FORMATION.” 2020. Web. 04 Mar 2021.

Vancouver:

Quiroz V. THE DEVELOPMENT OF AN H1 EMBRYONIC STEM CELL LINE TO STUDY THE ROLE OF THE ONCOGENES LMO1 AND MYCN IN HUMAN NEUROBLASTOMA FORMATION. [Internet] [Thesis]. California State University – San Bernardino; 2020. [cited 2021 Mar 04]. Available from: https://scholarworks.lib.csusb.edu/etd/1125.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Quiroz V. THE DEVELOPMENT OF AN H1 EMBRYONIC STEM CELL LINE TO STUDY THE ROLE OF THE ONCOGENES LMO1 AND MYCN IN HUMAN NEUROBLASTOMA FORMATION. [Thesis]. California State University – San Bernardino; 2020. Available from: https://scholarworks.lib.csusb.edu/etd/1125

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

30. Feeney, Meghan Margaret. Two Distinct Populations of Urinary Pacemaker Cells Arise From The Neural Crest.

Degree: 2014, University of Toronto

URL: http://hdl.handle.net/1807/73825

►

Two distinct populations of urinary pacemaker cells (PMCs), marked by HCN3 and C-KIT respectively, control ureteric peristalsis to propel urine from the kidney to the… (more)

Subjects/Keywords: C-kit; Hcn3; Neural Crest; Renal Devleopment; Urinary Pacemaker Cells; 0758

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Feeney, M. M. (2014). Two Distinct Populations of Urinary Pacemaker Cells Arise From The Neural Crest. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/73825

Chicago Manual of Style (16^th Edition):

Feeney, Meghan Margaret. “Two Distinct Populations of Urinary Pacemaker Cells Arise From The Neural Crest.” 2014. Masters Thesis, University of Toronto. Accessed March 04, 2021. http://hdl.handle.net/1807/73825.

MLA Handbook (7^th Edition):

Feeney, Meghan Margaret. “Two Distinct Populations of Urinary Pacemaker Cells Arise From The Neural Crest.” 2014. Web. 04 Mar 2021.

Vancouver:

Feeney MM. Two Distinct Populations of Urinary Pacemaker Cells Arise From The Neural Crest. [Internet] [Masters thesis]. University of Toronto; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1807/73825.

Council of Science Editors:

Feeney MM. Two Distinct Populations of Urinary Pacemaker Cells Arise From The Neural Crest. [Masters Thesis]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/73825

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