Border cells are an in vivo model for collective cell migration. Here, we identify the gene cactin as essential for border cell cluster organization, delamination, and migration. In Cactin-depleted cells, the apical proteins aPKC and Crumbs (Crb) become abnormally concentrated, and overall cluster polarity is lost. Apically tethering excess aPKC is sufficient to cause delamination defects, and relocalizing apical aPKC partially rescues delamination. Cactin is conserved from yeast to humans and has been implicated in diverse processes. In border cells, Cactin’s evolutionarily conserved spliceosome function is required. Whole transcriptome analysis revealed alterations in isoform expression in Cactin-depleted cells. Mutations in two affected genes, Sec23 and Sec24CD, which traffic Crb to the apical cell surface, partially rescue border cell cluster organization and migration. Overexpression of Rab5 or Rab11, which promote Crb and aPKC recycling, similarly rescues. Thus, a general splicing factor is specifically required for coordination of cluster polarity and migration, and migrating border cells are particularly sensitive to splicing and cell polarity disruptions.

中文翻译：

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边界细胞极性和集体迁移需要剪接体成分仙人掌

边界细胞是集体细胞迁移的体内模型。在这里，我们确定仙人掌基因对于边界细胞簇的组织、分层和迁移至关重要。在仙人掌蛋白耗尽的细胞中，顶端蛋白 aPKC 和 Crumbs (Crb) 变得异常集中，并且整体簇极性丢失。顶端束缚过量的 aPKC 足以导致分层缺陷，而重新定位顶端 aPKC 可以部分挽救分层。仙人掌从酵母到人类都是保守的，并且与多种过程有关。在边缘细胞中，需要仙人掌在进化上保守的剪接体功能。全转录组分析揭示了仙人掌蛋白耗尽细胞中异构体表达的变化。两个受影响基因 Sec23 和 Sec24CD 的突变将 Crb 运输到顶端细胞表面，部分挽救了边缘细胞簇的组织和迁移。 Rab5 或 Rab11 的过度表达可促进 Crb 和 aPKC 的回收，同样可以起到拯救作用。因此，协调簇极性和迁移特别需要通用剪接因子，并且迁移边界细胞对剪接和细胞极性破坏特别敏感。