The apical determinants aPKC and dPatj regulate Frizzled-dependent planar cell polarity in the Drosophila eye
The apical determinants aPKC and dPatj regulate Frizzled-dependent planar cell polarity in the Drosophila eye
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DOI：
10.1016/j.cell.2005.03.014
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发表时间：
2005-05-20
期刊：
影响因子：
64.5
通讯作者：
Mlodzik, M
中科院分区：
文献类型：
--
作者：
Djiane, A;Yogev, S;Mlodzik, M
平面细胞极性（PCP）是许多脊椎动物和无脊椎动物上皮的共同特征，垂直于它们的顶/基（a /B）极性轴。虽然PCP决定因子如frizzed （Fz1）的根尖定位对其功能至关重要，但人们对A/B极性与PCP之间的联系知之甚少。在这里，我们描述了a /B决定因素与fz1介导的果蝇眼睛PCP建立之间的直接分子联系。我们证明dPatj结合Fz1的细胞质尾部，并提出它招募aPKC， aPKC反过来磷酸化并抑制Fz1。因此，aPKC复合物和dPatj的组分在眼睛中产生PCP缺陷。我们还发现，在PCP信号传导过程中，aPKC和dPatj下调，而Bazooka上调，表明Bazooka对dPatj/aPKC具有拮抗作用。我们提出了一个模型，其中dPatj/aPKC复合物通过抑制细胞中不应活跃的Fz1来调节PCP。
Planar cell polarity (PCP) is a common feature of many vertebrate and invertebrate epithelia and is perpendicular to their apical/basal (A/B) polarity axis. While apical localization of PCP determinants such as Frizzled (Fz1) is critical for their function, the link between A/B polarity and PCP is poorly understood. Here, we describe a direct molecular link between A/B determinants and Fz1-mediated PCP establishment in the Drosophila eye. We demonstrate that dPatj binds the cytoplasmic tail of Fz1 and propose that it recruits aPKC, which in turn phosphorylates and inhibits Fz1. Accordingly, components of the aPKC complex and dPatj produce PCP defects in the eye. We also show that during PCP signaling, aPKC and dPatj are downregulated, while Bazooka is upregulated, suggesting an antagonistic effect of Bazooka on dPatj/aPKC. We propose a model whereby the dPatj/aPKC complex regulates PCP by inhibiting Fz1 in cells where it should not be active.