Characterization of MP2 cell division and pins function on spindle asymmetry of drosophila central nervous system
LIN SHUPING
LIN SHUPING
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Abstract
Asymmetric cell division is a fundamental and universal process of generating cell diversity during animal development. Drosophila melanogaster provides an excellent model for understanding the mechanisms of asymmetric cell division. In chapter 3, I described the characterization of MP2 cell division. I analyzed the MP2 cell division in great detail and found that inscuteable mutations had no effect on the sibling cell fate specification this lineage. In contrast, Notch-like cell fate transformations were observed in loss-of-funciton mutations of bazooka(95%) and pins(15%). Thus our findings, that a specific neuroblast lineage shows inscuteable-independent asymmetry, provide a novel perspective on asymmetric cell division. In chapter 4, I demonstrate that GI?13F NB similar-sized division phenotype is due to the cortical Pins/GI?i. When Pins or GI?i is further removed from the GI?13F NBs, the similar-sized NB division phenotype is rescued. The chimeric Pins-C-Pon is uniformly cortical in most mitotic NBs and mimics cortical Pins/GI?i to produce two daughter cells with similar size. In the absence of GI?i, ectopic expression of GI?o can recruit Pins to the cortical cortex and disrupt spindle asymmetry(90%). So taken together, GI?i functions through Pins to play a role in spindle asymmetry and Pins is the real player.In chapter 5, I described an interesting phenotype in embryos overexpressing GI?i or GI?o. In WT, spindle pole positions always overlie with the apical protein crescent and basal protein crescent. However, in embryos overexpressing GI?i(37.5%) or GI?o(50%), the crescent of basal protein does not overlie with one of the spindles poles during metaphase and basal protein such as Mir is bisected into two daughter cells. Here I define this phenotype as a??spindle uncouplinga??.
Keywords
MP2, Baz, Insc-independent, Pins, Spindle asymmetry, Spindle uncoupling
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Date
2006-11-01
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