Redox-sensitive CDC-42 clustering promotes wound closure in C. elegans
Jingxiu Xu, Xinan Meng, Qingxian Yang, Jianqin Zhang, Wei Hu, Hongying Fu, Jack Wei Chen, Weirui Ma, Andrew D. Chisholm, Qiming Sun, Suhong Xu
Journal：Cell Reports
IF：9.42
DOI：10.1016/j.celrep.2021.110040
PMID：34818546
Published：2021-11-23
research field：分子生物学细胞生物学发育生物学
Abstract
Summary Tissue damage induces immediate-early signals, activating Rho small GTPases to trigger actin polymerization essential for later wound repair. However, how tissue damage is sensed to activate Rho small GTPases locally remains elusive. Here, we found that wounding the C. elegans epidermis induces rapid relocalization of CDC-42 into plasma membrane-associated clusters, which subsequently recruits WASP/WSP-1 to trigger actin polymerization to close the wound. In addition, wounding induces a local transient increase and subsequent reduction of H 2 O 2 , which negatively regulates the clustering of CDC-42 and wound closure. CDC-42 CAAX motif-mediated prenylation and polybasic region-mediated cation-phospholipid interaction are both required for its clustering. Cysteine residues participate in intermolecular disulfide bonds to reduce membrane association and are required for negative regulation of CDC-42 clustering by H 2 O 2 . Collectively, our findings suggest that H 2 O 2 -regulated fine-tuning of CDC-42 localization can create a distinct biomolecular cluster that facilitates rapid epithelial wound repair after injury.
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