The mitotic-to-endocycle switch in Drosophila follicle cells is executed by Notch-dependent regulation of G1/S, G2/M and M/G1 cell-cycle transitions.

摘要: The Notch signaling pathway controls the follicle cell mitotic-to-endocycle transition in Drosophila oogenesis by stopping mitotic cycle and promoting endocycle. To understand how coordinates this process, we have identified performed a functional analysis of genes whose transcription is responsive to at transition. These include G2/M regulator Cdc25 phosphatase, String; APC ubiquitination complex Hec/CdhFzr an inhibitor CyclinE/CDK complex, Dacapo. activity leads downregulation String Dacapo, activation Fzr. All three are independently Notch. In addition, CdhFzr, essential gene for endocycles, sufficient stop promote precocious endocycles when expressed prematurely during stages. contrast, overexpression growth controller Myc does not induce premature but accelerates kinetics normal endocycles. We also show that Archipelago (Ago), SCF-regulator dispensable mitosis, crucial endocycle progression epithelium. results support model which executes switch regulating all major transitions. Repression blocks M-phase, Fzr allows G1 repression Dacapo assures entry into S-phase. This study provides comprehensive picture logic external pathways may use control transitions coordinated regulation cycle.