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首页> 外文期刊>Current Biology: CB >Aurora A Triggers Lgl Cortical Release during Symmetric Division to Control Planar Spindle Orientation
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Aurora A Triggers Lgl Cortical Release during Symmetric Division to Control Planar Spindle Orientation

机译：Aurora A在对称分割过程中触发Lgl皮质释放以控制平面主轴的方向

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Mitotic spindle orientation is essential to control cell-fate specification and epithelial architecture [1]. The tumor suppressor Lgl localizes to the basolateral cortex of epithelial cells, where it acts together with Dlg and Scrib to organize apicobasal polarity [2]. Dlg and Scrib also control planar spindle orientation [3, 4], but how the organization of polarity complexes is adjusted to control symmetric division is largely unknown. Here, we show that the Dlg complex is remodeled during Drosophila follicular epithelium cell division, when Lgl is released to the cytoplasm. Lgl redistribution during epithelial mitosis is reminiscent of asymmetric cell division, where it is proposed that Aurora A promotes aPKC activation to control the localization of Lgl and cell-fate determinants [5]. We show that Aurora A controls Lgl localization directly, triggering its cortical release at early prophase in both epithelial and S2 cells. This relies on double phosphorylation within the putative aPKC phosphorylation site, which is required and sufficient for Lgl cortical release during mitosis and can be achieved by a combination of aPKC and Aurora A activities. Cortical retention of Lgl disrupts planar spindle orientation, but only when Lgl mutants that can bind Dlg are expressed. Hence, our work reveals that Lgl mitotic cortical release is not specifically linked to the asymmetric segregation of fate determinants, and we propose that Aurora A activation breaks the Dlg/Lgl interaction to allow planar spindle orientation during symmetric division via the Pins (LGN)/Dlg pathway.
机译：有丝分裂纺锤体定向对于控制细胞命运的规范和上皮结构至关重要[1]。肿瘤抑制因子Lgl定位于上皮细胞的基底外侧皮层，在这里它与Dlg和Scrib共同起作用，以组织成末梢极性[2]。 Dlg和Scrib也可以控制平面主轴的方向[3，4]，但是如何调整极性复合物的结构以控制对称分割仍然未知。在这里，我们显示了当Lgl释放到细胞质中时，果蝇滤泡上皮细胞分裂过程中Dlg复合物被重塑。 Lgl在上皮有丝分裂过程中的重新分布使人联想到不对称细胞分裂，有人提出Aurora A促进aPKC活化以控制Lgl和细胞命运决定因素的定位[5]。我们显示，Aurora A直接控制Lgl定位，在上皮细胞和S2细胞的早期前期触发其皮质释放。这依赖于假定的aPKC磷酸化位点内的双重磷酸化，这对于有丝分裂期间Lgl皮质的释放是必需的并且是足够的，并且可以通过aPKC和Aurora A活性的组合来实现。 Lgl的皮质保留会破坏平面纺锤体定向，但仅当表达可以结合Dlg的Lgl突变体时才如此。因此，我们的工作表明，Lgl有丝分裂皮质的释放与命运决定因素的不对称分离没有特定联系，我们提出Aurora A激活会破坏Dlg / Lgl相互作用，从而在通过销子（LGN）/ Dlg途径。

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