Epithelial cells undergo cortical rounding at the onset of mitosis to enable spindle orientation in the plane of the epithelium. In cuboidal epithelia in culture, the adherens junction protein E-cadherin recruits Pins/LGN/GPSM2 and Mud/NuMA to orient the mitotic spindle. In the pseudostratified columnar epithelial cells of Drosophila, septate junctions recruit Mud/NuMA to orient the spindle, while Pins/LGN/GPSM2 is surprisingly dispensable. We show that these pseudostratified epithelial cells downregulate E-cadherin as they round up for mitosis. Preventing cortical rounding by inhibiting Rho-kinase-mediated actomyosin contractility blocks downregulation of E-cadherin during mitosis. Mitotic activation of Rho-kinase depends on the RhoGEF ECT2/Pebble and its binding partners RacGAP1/MgcRacGAP/CYK4/Tum and MKLP1/KIF23/ZEN4/Pav. Cell cycle control of these Rho activators is mediated by the Aurora A and B kinases, which act redundantly during mitotic rounding. Thus, in Drosophila pseudostratified epithelia, disruption of adherens junctions during mitosis necessitates planar spindle orientation by septate junctions to maintain epithelial integrity.

中文翻译：

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假复层上皮细胞有丝分裂变圆过程中粘附连接重塑。


上皮细胞在有丝分裂开始时经历皮质变圆，以使纺锤体能够在上皮平面内定向。在培养的立方上皮中，粘附连接蛋白 E-钙粘蛋白招募 Pins/LGN/GPSM2 和 Mud/NuMA 来定向有丝分裂纺锤体。在果蝇的假复层柱状上皮细胞中，隔膜连接招募 Mud/NuMA 来定向纺锤体，而 Pins/LGN/GPSM2 却是可有可无的。我们发现，这些假复层上皮细胞在进行有丝分裂时下调 E-钙粘蛋白。通过抑制 Rho 激酶介导的肌动球蛋白收缩性来防止皮质变圆，可阻止有丝分裂期间 E-钙粘蛋白的下调。 Rho 激酶的有丝分裂激活取决于 RhoGEF ECT2/Pebble 及其结合伙伴 RacGAP1/MgcRacGAP/CYK4/Tum 和 MKLP1/KIF23/ZEN4/Pav。这些 Rho 激活剂的细胞周期控制是由 Aurora A 和 B 激酶介导的，它们在有丝分裂过程中发挥着冗余作用。因此，在果蝇假复层上皮中，有丝分裂期间粘附连接的破坏需要通过隔膜连接进行平面纺锤体定向以维持上皮完整性。