Proteins of the ezrin, radixin, and moesin (ERM) family control cell and tissue morphogenesis. We previously reported that moesin, the only ERM in Drosophila, controls mitotic morphogenesis and epithelial integrity. We also found that the Pp1-87B phosphatase dephosphorylates moesin, counteracting its activation by the Ste20-like kinase Slik. To understand how this signaling pathway is itself regulated, we conducted a genome-wide RNAi screen, looking for new regulators of moesin activity. We identified that Slik is a new member of the striatin-interacting phosphatase and kinase complex (STRIPAK). We discovered that the phosphatase activity of STRIPAK reduces Slik phosphorylation to promote its cortical association and proper activation of moesin. Consistent with this finding, inhibition of STRIPAK phosphatase activity causes cell morphology defects in mitosis and impairs epithelial tissue integrity. Our results implicate the Slik–STRIPAK complex in the control of multiple morphogenetic processes.

中文翻译：

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STRIPAK 调节 Slik 定位以控制有丝分裂形态发生和上皮完整性

埃兹蛋白、根蛋白和模蛋白 (ERM) 家族的蛋白质控制细胞和组织的形态发生。我们之前报道过，moesin 是果蝇中唯一的 ERM，控制有丝分裂形态发生和上皮完整性。我们还发现 Pp1-87B 磷酸酶使 moesin 去磷酸化，抵消 Ste20 样激酶 Slik 对其的激活。为了了解这一信号通路本身是如何调节的，我们进行了全基因组 RNAi 筛选，寻找新的 moesin 活性调节因子。我们确定 Slik 是 striatin 相互作用磷酸酶和激酶复合物 (STRIPAK) 的新成员。我们发现 STRIPAK 的磷酸酶活性可降低 Slik 磷酸化，从而促进其皮质关联和 moesin 的正确激活。与这一发现一致，抑制 STRIPAK 磷酸酶活性会导致有丝分裂中的细胞形态缺陷并损害上皮组织完整性。我们的结果表明 Slik-STRIPAK 复合物参与多种形态发生过程的控制。