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After the relief of ureteric obstruction, Rac1 promoted actin cytoskeletal reconstitution, which was required to maintain normal mitotic morphology allowing for successful cell division. Mechanistically, Rac1 restricted excessive actomyosin activity that stabilized the negative mitotic entry kinase Wee1. This mechanism ensured mechanical G\n            <jats:sub>2<\/jats:sub>\n            -M checkpoint stability and prevented premature mitotic entry. The repair defects following injury could be rescued by direct myosin inhibition. Thus, Rac1-dependent control of the actin cytoskeleton integrates with the cell cycle to mediate kidney tubular repair by preventing dysmorphic cells from entering cell division.\n          <\/jats:p>","DOI":"10.1126\/sciadv.adi7840","type":"journal-article","created":{"date-parts":[[2024,2,7]],"date-time":"2024-02-07T19:36:41Z","timestamp":1707334601000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":19,"title":["Rac1 promotes kidney collecting duct repair by mechanically coupling cell morphology to mitotic entry"],"prefix":"10.1126","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0788-2945","authenticated-orcid":true,"given":"Fabian","family":"Bock","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA."},{"name":"Department of Veterans Affairs Hospital, Tennessee Valley Healthcare System, 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