The tumor-suppressor and cell adhesion molecule Fat controls planar polarity via physical interactions with Atrophin, a transcriptional co-repressor
The tumor-suppressor and cell adhesion molecule Fat controls planar polarity via physical interactions with Atrophin, a transcriptional co-repressor
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DOI：
10.1242/dev.00304
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发表时间：
2003-02-01
期刊：
影响因子：
4.6
通讯作者：
McNeill, H
中科院分区：
文献类型：
--
作者：
Fanto, M;Clayton, L;McNeill, H
脂肪是一种非典型的钙粘蛋白，控制细胞生长和平面极性。Atrophin是一种核辅阻遏物，也是平面极性所必需的;然而，目前尚不清楚Atrophin在平面极性中控制什么基因，或者Atrophin活性在平面极性建立期间如何调节。我们发现，Atrophin结合到脂肪的胞质结构域和Atrophin突变体显示出强大的遗传相互作用与脂肪。我们发现，Atrophin和脂肪克隆在眼睛中有非自主的中断平面极性，仅限于克隆的极性边界，并有救援的平面极性缺陷的赤道边界上的这些克隆。脂肪和Atrophin都需要控制四关节表达。此外，我们的镶嵌分析表明，增强的需求，在R3感光细胞的Atrophin。这些数据使我们建立了一个模型，其中脂肪和Atrophin在确定眼睛的平面极性时起两次作用：首先通过产生平面极性扩散信号建立位置信息，然后确定R3命运。
Fat is an atypical cadherin that controls both cell growth and planar polarity. Atrophin is a nuclear co-repressor that is also essential for planar polarity; however, it is not known what genes Atrophin controls in planar polarity, or how Atrophin activity is regulated during the establishment of planar polarity. We show that Atrophin binds to the cytoplasmic domain of Fat and that Atrophin mutants show strong genetic interactions with fat. We find that both Atrophin and fat clones in the eye have non-autonomous disruptions in planar polarity that are restricted to the polar border of clones and that there is rescue of planar polarity defects on the equatorial border of these clones. Both fat and Atrophin are required to control four-jointed expression. In addition our mosaic analysis demonstrates an enhanced requirement for Atrophin in the R3 photoreceptor. These data lead us to a model in which fat and Atrophin act twice in the determination of planar polarity in the eye: first in setting up positional information through the production of a planar polarity diffusible signal, and later in R3 fate determination.