Notch signaling through Tramtrack bypasses the mitosis promoting activity of the JNK pathway in the mitotic-to-endocycle transition of Drosophila follicle cells

被引:38
作者
Jordan, KC [1 ]
Schaeffer, V [1 ]
Fischer, KA [1 ]
Gray, EE [1 ]
Ruohola-Baker, H [1 ]
机构
[1] Univ Washington, Dept Biochem, Seattle, WA 98195 USA
来源
BMC DEVELOPMENTAL BIOLOGY | 2006年 / 6卷
关键词
D O I
10.1186/1471-213X-6-16
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Background: The follicle cells of the Drosophila egg chamber provide an excellent model in which to study modulation of the cell cycle. During mid-oogenesis, the follicle cells undergo a variation of the cell cycle, endocycle, in which the cells replicate their DNA, but do not go through mitosis. Previously, we showed that Notch signaling is required for the mitotic-to-endocycle transition, through downregulating String/Cdc25, and Dacapo/p21 and upregulating Fizzy-related/Cdh1. Results: In this paper, we show that Notch signaling is modulated by Shaggy and temporally induced by the ligand Delta, at the mitotic-to-endocycle transition. In addition, a downstream target of Notch, tramtrack, acts at the mitotic-to-endocycle transition. We also demonstrate that the JNK pathway is required to promote mitosis prior to the transition, independent of the cell cycle components acted on by the Notch pathway. Conclusion: This work reveals new insights into the regulation of Notch-dependent mitotic-to-endocycle switch.
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页数:12
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