Please use this identifier to cite or link to this item:
https://scholarbank.nus.edu.sg/handle/10635/142003
DC Field | Value | |
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dc.title | THE INTRINSIC MECHANISMS FOR SELF-RENEWAL OF DROSOPHILA STEM CELLS | |
dc.contributor.author | YANG YING | |
dc.date.accessioned | 2018-05-15T18:00:27Z | |
dc.date.available | 2018-05-15T18:00:27Z | |
dc.date.issued | 2018-01-23 | |
dc.identifier.citation | YANG YING (2018-01-23). THE INTRINSIC MECHANISMS FOR SELF-RENEWAL OF DROSOPHILA STEM CELLS. ScholarBank@NUS Repository. | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/142003 | |
dc.description.abstract | Stem cells have the potential to maintain the undifferentiated state and differentiate into specialized cell types. The germline stem cells and Neuroblasts of the Drosophila have been proven to be powerful platforms for studying stem cell maintenance and differentiation. I have identified that disruption of CG4078 function leads to premature loss of GSC. Interestingly, I have observed GSC conversion to hub cells in mutant CG4078 testis. Further investigation of CG4078 function reveals that CG4078 is possibly involved in genomic stability maintenance. The RNA-seq data illustrates that genes involved in GSC self-renewal and differentiation are reduced in CG4078 mutant testis. Besides, I showed that the direct interaction between Mira and Stau dsRBD5 is essential for asymmetric distribution of Stau in Drosophila larva brain. Moreover, I showed that Pon promotes larval NB differentiation upstream of the Numb-Notch axis, and the Numb/Pon interaction is essential for Pon function during ACD of NBs. | |
dc.language.iso | en | |
dc.subject | GSC, Neuroblast, dRTEL1, Mira, Numb, Drosophila | |
dc.type | Thesis | |
dc.contributor.department | BIOLOGICAL SCIENCES | |
dc.contributor.supervisor | Cai Yu | |
dc.description.degree | Ph.D | |
dc.description.degreeconferred | DOCTOR OF PHILOSOPHY (FOS) | |
dc.identifier.orcid | 0000-0002-2032-9183 | |
Appears in Collections: | Ph.D Theses (Open) |
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YangY.pdf | 8.13 MB | Adobe PDF | OPEN | None | View/Download |
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