ARVCF catenin controls force production during vertebrate convergent extension.

ARVCF catenin controls force production during vertebrate convergent extension.
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DOI:
10.1016/j.devcel.2022.04.001
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发表时间:
2022-05-09
期刊:
影响因子:
11.8
通讯作者:
Wallingford, John B.
Wallingford, John B.
中科院分区:
生物学1区
文献类型:
--
作者:
Huebner, Robert J.;Weng, Shinuo;Lee, Chanjae;Sarikaya, Sena;Papoulas, Ophelia;Cox, Rachael M.;Marcotte, Edward M.;Wallingford, John B.

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动物身体计划的设计是在基因组中编码的,这个程序的执行是一个涉及蛋白质、细胞和整个组织协调运动的机械过程。因此,理解形态发生的一个挑战是将发生在不同长度尺度上的事件联系起来。在这里,我们描述了一个特性不佳的粘附效应,Arvcf catenin,如何控制爪蟾从头到尾的轴延伸。我们发现,在完整的生物体中,Arvcf是轴延伸所必需的,而在分离的组织中则不是。我们表明,有机体的规模表型是由组织规模力生产的缺陷造成的。最后,我们确定力缺陷是由于抑制了细胞粘附和细胞骨架蛋白向膜的脉动性募集。这些结果提供了对轴扩展过程中Arvcf功能的全面理解,并深入了解细胞尺度的粘附缺陷如何导致生物尺度的发育失败。
The design of an animal’s body plan is encoded in the genome and execution of this program is a mechanical progression involving coordinated movement of proteins, cells, and whole tissues. Thus, a challenge to understanding morphogenesis is connecting events that occur across various length scales. Here, we describe how a poorly characterized adhesion effector, Arvcf catenin, controls Xenopus head-to-tail axis extension. We find that Arvcf is required for axis extension within the intact organism but not within isolated tissues. We show that the organism scale phenotype results from a defect in tissue scale force production. Finally, we determine that the force defect results from dampening of the pulsatile recruitment of cell adhesion and cytoskeletal proteins to membranes. These results provide a comprehensive understanding of Arvcf function during axis extension and produce insight into how a cellular scale defect in adhesion results in an organism scale failure of development.
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