Jordan Katherine C, Schaeffer Valerie, Fischer Karin A, Gray Elizabeth E, Ruohola-Baker Hannele
Department of Biochemistry, University of Washington, Box 357350, Seattle, WA 98195, USA.
BMC Dev Biol. 2006 Mar 16;6:16. doi: 10.1186/1471-213X-6-16.
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.
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.
This work reveals new insights into the regulation of Notch-dependent mitotic-to-endocycle switch.
果蝇卵室的滤泡细胞为研究细胞周期调控提供了一个绝佳模型。在卵子发生中期，滤泡细胞经历细胞周期的一种变体——内复制周期，其中细胞复制其DNA，但不进行有丝分裂。此前，我们表明Notch信号传导通过下调String/Cdc25和Dacapo/p21并上调Fizzy-related/Cdh1，对于有丝分裂向内复制周期的转变是必需的。
在本文中，我们表明Notch信号传导在有丝分裂向内复制周期转变时受Shaggy调节，并由配体Delta在时间上诱导。此外，Notch的一个下游靶点tramtrack在有丝分裂向内复制周期转变时起作用。我们还证明JNK途径在转变之前促进有丝分裂是必需的，这独立于Notch途径作用的细胞周期成分。
这项工作揭示了对Notch依赖性有丝分裂向内复制周期转换调控的新见解。
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