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Traf4 在极化黏附连接中的作用作为有效细胞形态变化的前提。

Role for Traf4 in polarizing adherens junctions as a prerequisite for efficient cell shape changes.

机构信息

Institute of Genetics, University of Cologne, Zülpicher Strasse 47, 50674 Cologne, Germany.

出版信息

Mol Cell Biol. 2011 Dec;31(24):4978-93. doi: 10.1128/MCB.05542-11. Epub 2011 Oct 10.

Abstract

Apical constriction of epithelial cells is a widely used morphogenetic mechanism. In the Drosophila embryo, the apical constrictions that internalize the mesoderm are controlled by the transcription factor Twist and require intact adherens junctions and a contractile acto-myosin network. We find that adherens junctions in constricting mesodermal cells undergo extensive remodeling. A Twist target gene encoding a member of the tumor necrosis factor (TNF) receptor-associated factor (TRAF) family, Traf4, is involved in this process. While TRAFs are best known for their functions in inflammatory responses, Traf4 appears to have a different role, and its mechanism of action is poorly understood. We show that Traf4 is required for efficient apical constriction during ventral furrow formation and for proper localization of Armadillo to the apical position in constricting cells. Traf4 and Armadillo interact with each other physically and functionally. Traf4 acts in a TNF receptor- and Jun N-terminal protein kinase (JNK)-independent manner to fine-tune the assembly of adherens junctions in the invaginating mesodermal cells.

摘要

上皮细胞的顶端缢缩是一种广泛使用的形态发生机制。在果蝇胚胎中,内化中胚层的顶端缢缩受转录因子 Twist 的控制,需要完整的黏着连接和收缩性的肌动球蛋白网络。我们发现,在进行顶端缢缩的中胚层细胞中,黏着连接经历了广泛的重塑。一个编码肿瘤坏死因子(TNF)受体相关因子(TRAF)家族成员的 Twist 靶基因 Traf4 参与了这个过程。虽然 TRAFs 以其在炎症反应中的功能而闻名,但 Traf4 似乎具有不同的作用,其作用机制尚不清楚。我们发现 Traf4 对于腹侧沟形成过程中的有效顶端缢缩以及 Armadillo 在收缩细胞中的顶端定位是必需的。Traf4 和 Armadillo 在物理和功能上相互作用。Traf4 以 TNF 受体和 Jun N 末端蛋白激酶(JNK)非依赖性的方式发挥作用,精细调节了内陷的中胚层细胞中黏着连接的组装。

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