ARHGEF17/TEM4 regulates the cell cycle through control of G1 progression

细胞生物学 有丝分裂 生物 细胞周期 鸟嘌呤核苷酸交换因子 罗亚 细胞周期蛋白 肌动蛋白细胞骨架 细胞周期蛋白B 细胞周期蛋白B1 细胞 GTP酶 细胞周期蛋白 细胞周期蛋白依赖激酶1 信号转导 细胞骨架 遗传学
作者
Diogjena Katerina Prifti,Annie Lauzier,Chantal Garand,Eva Calvo,Romain Devillers,Suparba Roy,Alexsandro dos Santos,Laurence Descombes,Benjamin Trudel,Mathieu Laplante,François Bordeleau,Sabine Elowe
出处
期刊:Journal of Cell Biology [The Rockefeller University Press]
卷期号:224 (3)
标识
DOI:10.1083/jcb.202311194
摘要

The Ras homolog (Rho) small GTPases coordinate diverse cellular functions including cell morphology, adhesion and motility, cell cycle progression, survival, and apoptosis via their role in regulating the actin cytoskeleton. The upstream regulators for many of these functions are unknown. ARHGEF17 (also known as TEM4) is a Rho family guanine nucleotide exchange factor (GEF) implicated in cell migration, cell–cell junction formation, and the mitotic checkpoint. In this study, we characterize the regulation of the cell cycle by TEM4. We demonstrate that TEM4-depleted cells exhibit multiple defects in mitotic entry and duration, spindle morphology, and spindle orientation. In addition, TEM4 insufficiency leads to excessive cortical actin polymerization and cell rounding defects. Mechanistically, we demonstrate that TEM4-depleted cells delay in G1 as a consequence of decreased expression of the proproliferative transcriptional co-activator YAP. TEM4-depleted cells that progress through to mitosis do so with decreased levels of cyclin B as a result of attenuated expression of CCNB1. Importantly, cyclin B overexpression in TEM4-depleted cells largely rescues mitotic progression and chromosome segregation defects in anaphase. Our study thus illustrates the consequences of Rho signaling imbalance on cell cycle progression and identifies TEM4 as the first GEF governing Rho GTPase-mediated regulation of G1/S.

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