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Identifier 000438793
Title Studies of transcription factors contributing to Drosophila early neurogenesis
Alternative Title Μελέτη των μεταγραφικών παραγόντων που συμμετέχουν στην εμβρυονική νευρογένεση της Drosophila Melanogaster
Author Μασούρα, Μαργαρίτα Θ.
Thesis advisor Δελιδάκης, Χρήστος
Abstract Development of the central nervous system constitutes a highly complex process that requires precise spatiotemporal regulation. In Drosophila melanogaster, neurogenesis initiates at the embryo and continues until pupal stages. Embryonic neurogenesis begins at the stage 8 with the generation of neural progenitors, called neuroblasts. Neuroblasts derive from the ventral ectoderm and are specified through the process of Notch-mediated lateral inhibition. During this process, effectors of Notch pathway, called Enhancer of split E(spl) and the proneural genes are antagonizing, creating an intercellular feedback loop. As a result, specific neuroectodermal cells are singled out and induce the neural fate. Upon its generation, neuroblasts delaminate from the ectodermal sheet and undergo multiple rounds of asymmetrical divisions to self-renew and give rise to a ganglion mother cell (GMC). GMC divides once again, forming a pair of neurons and/or glia. Even though mechanisms implicated in lateral inhibition have been extensively studied, the complex interplay between proneural genes and Notch is yet to be fully resolved. Proneural genes encode bHLH transcriptional activators which heterodimerize with another bHLH factor, called Daughterless (Da), to promote induction of the neural fate. On the other hand, genes of the E(spl) locus encode bHLH transcriptional repressors that downregulate proneural activity and lead to epidermal specification. Mutations in E(spl) result in the development of neural hyperplasia. Whereas, absence of proneural genes leads to the partial loss of neuroblasts, accounting for 20-25%. Neuroblasts that manage to be formed exhibit a temporary pause of its divisions and lack expression of certain genes including deadpan (dpn). Divisions and dpn expression restart in later embryonic stages. The mechanisms implicated in this “stalled state” are yet to be uncovered. To better understand this process, we studied embryos lacking both proneurals and E(spl) genes referred as “double mutants”. We observe a hyperplastic phenotype with temporary arrest of neuroblast divisions and delayed dpn expression. We also studied the role of Da in the neuroectoderm. While mutations on either da or proneurals cause only a partial loss of neuroblasts, embryos lacking both are aneural. We wanted to examine if Da can activate distinct gene targets in the neuroectoderm in a proneural independent manner. Thus, we developed a cHIP-sequencing protocol to identify Da targets. Our technique is based on a biotin pull-down strategy for the precipitation of Da. We didn’t identify unique neural targets. However, we validated the efficiency of our protocol, which needs further optimization.
Language English
Subject Developmental neurobiology
Embryonic neurogenesis
Proneural factors
Αναπτυξιακή νευροβιολογία
Προνευρικοί παράγοντες
Issue date 2021-03-26
Collection   School/Department--School of Sciences and Engineering--Department of Biology--Post-graduate theses
  Type of Work--Post-graduate theses
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