Harris Tony J C, Peifer Mark
Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario, Canada.
Dev Cell. 2007 May;12(5):727-38. doi: 10.1016/j.devcel.2007.02.011.
Tissue morphogenesis requires assembling and disassembling individual cell-cell contacts without losing epithelial integrity. This requires dynamic control of adherens junction (AJ) positioning around the apical domain, but the mechanisms involved are unclear. We show that atypical Protein Kinase C (aPKC) is required for symmetric AJ positioning during Drosophila embryogenesis. aPKC is dispensable for initial apical AJ recruitment, but without aPKC, AJs form atypical planar-polarized puncta at gastrulation. Preceding this, microtubules fail to dissociate from centrosomes, and at gastrulation abnormally persistent centrosomal microtubule asters cluster AJs into the puncta. Dynein enrichment at the puncta suggests it may draw AJs and microtubules together and microtubule disruption disperses the puncta. Through cytoskeletal disruption in wild-type embryos, we find a balance of microtubule and actin interactions controls AJ symmetry versus planar polarity during normal gastrulation. aPKC apparently regulates this balance. Without aPKC, abnormally strong microtubule interactions break AJ symmetry and epithelial structure is lost.
组织形态发生需要在不丧失上皮完整性的情况下组装和拆卸单个细胞间连接。这需要动态控制黏着连接（AJ）在顶端区域周围的定位，但其涉及的机制尚不清楚。我们发现非典型蛋白激酶C（aPKC）在果蝇胚胎发育过程中对称AJ定位是必需的。aPKC对于初始顶端AJ募集并非必需，但没有aPKC时，AJ在原肠胚形成时形成非典型的平面极化斑点。在此之前，微管无法从中心体解离，并且在原肠胚形成时，异常持久的中心体微管星状体将AJ聚集到斑点中。斑点处动力蛋白的富集表明它可能将AJ和微管拉到一起，而微管破坏会分散斑点。通过野生型胚胎中的细胞骨架破坏，我们发现在正常原肠胚形成过程中，微管和肌动蛋白相互作用的平衡控制着AJ的对称性与平面极性。aPKC显然调节这种平衡。没有aPKC时，异常强烈的微管相互作用会破坏AJ对称性并导致上皮结构丧失。
