Apical PAR complex proteins protect against programmed epithelial assaults to create a continuous and functional intestinal lumen.
Apical PAR complex proteins protect against programmed epithelial assaults to create a continuous and functional intestinal lumen.
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DOI：
10.7554/elife.64437
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发表时间：
2021-06-17
期刊：
影响因子：
7.7
通讯作者：
Feldman JL
中科院分区：
文献类型：
--
作者：
Sallee MD;Pickett MA;Feldman JL
上皮细胞的持续极性和粘附性对于保护我们的器官和身体是必不可少的，这种上皮完整性是在器官发育过程中出现的，在无数的程序性形态发生攻击中出现。以发育中的秀丽隐杆线虫肠道为活体模型，研究了上皮细胞如何通过细胞分裂和伸长来构建功能管来保持其完整性。活体成像显示，在有丝分裂过程中，顶端PAR复合体蛋白PAR-6/Par6和PKC-3/aPKC保持在顶端，而顶端微管和微管组织中心(MTOC)蛋白被暂时去除。肠道特异性的PAR-6、PKC-3和aPKC调节因子CDC-42/CDC42的缺失导致了顶端MTOC以及细胞分裂后其他顶端和连接蛋白以及伸长的未分裂细胞中的持续间隙。在孵化时，缝隙与管腔狭窄相吻合，阻碍了食物，幼虫被捕获并死亡。因此，心尖PAR复合体维持心尖和连接的连续性，以构建一个功能正常的肠管。
Sustained polarity and adhesion of epithelial cells is essential for the protection of our organs and bodies, and this epithelial integrity emerges during organ development amidst numerous programmed morphogenetic assaults. Using the developing Caenorhabditis elegans intestine as an in vivo model, we investigated how epithelia maintain their integrity through cell division and elongation to build a functional tube. Live imaging revealed that apical PAR complex proteins PAR-6/Par6 and PKC-3/aPkc remained apical during mitosis while apical microtubules and microtubule-organizing center (MTOC) proteins were transiently removed. Intestine-specific depletion of PAR-6, PKC-3, and the aPkc regulator CDC-42/Cdc42 caused persistent gaps in the apical MTOC as well as in other apical and junctional proteins after cell division and in non-dividing cells that elongated. Upon hatching, gaps coincided with luminal constrictions that blocked food, and larvae arrested and died. Thus, the apical PAR complex maintains apical and junctional continuity to construct a functional intestinal tube.