| Summary: | 碩士 === 國立臺灣大學 === 動物學研究所 === 89 === Programmed cell death and cell migration are essential phenomenon in animal development. I took the advantages of C. elegans to study the relationship between ced-2, ced-5, ced-10, ced-12 , four genes which play important roles in both cell corpse engulfment and distal-tip cell migration. After genetic and molecular analyses, I found that ced-12 functions in the pathway mediated by ced-2, ced-5, ced-10 but not by ced-1, ced-6, ced-7 and that CED-5 can interact with CED-10 and CED-12 in vivo. These results in combination with the finding that ced-10 acts downstream of ced-2, ced-5, and ced-12 by Reddien, Horviz, Tsai and Wu, and that CED-2, CED-5 and CED-12 can form a ternary complex suggest that the big CED-2/CED-5/CED-12 complex may be important in activation of CED-10 and conserved with mammalian CrkII/DOCK180/Rac pathway which is important in cytoskeleton rearrangement. The mig-2(mu28) mutation alone does not alter the engulfment of cell corpses but indeed enhances the engulfment defect in the ced-2, ced-5, ced-10, ced-12 mutant backgrounds. This result suggests that mig-2 may play a redundant role with ced-2, ced-5, ced-10, ced-12 in the engulfment process. The enhancement in the DTC-migration defect in ced-12 mutant is also observed in the ced-2 and ced-10 mutant backgrounds but not in the ced-5 backgrounds. This result suggests that ced-5 maybe a branch point in the DTC migration path. unc-73 encodes a GEF which can catalyze the mammalian Rac1 in vitro. Overexpression of unc-73B which contains only the first DH domain can rescue the Ced-12 DTC-migration defect. These data together suggest that ced-12 may activate ced-10 through unc-73 during DTC migration.
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