ArticleThe Journal of cell biology2021
Rac1 promotes kidney collecting duct integrity by limiting actomyosin activity.
Article in The Journal of cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- α-Parvin regulation of cell rearrangement is critical for ureteric bud branching morphogenesis.Science advances · 2026Article
- Kindlins regulate integrin- and growth factor-dependent ureteric bud formation.Development (Cambridge, England) · 2026Article
- Epithelial cell shape changes contribute to regulation of ureteric bud branching morphogenesis.The FEBS journal · 2025Article
- Rac1 promotes proximal tubule kidney repair by coupling the actin cytoskeleton to mitochondrial function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Integrins in the kidney - beyond the matrix.Nature reviews. Nephrology · 2025Review
- Advancements in therapeutic development: kidney organoids and organs on a chip.Kidney international · 2024Review
- Rac1 promotes kidney collecting duct repair by mechanically coupling cell morphology to mitotic entry.Science advances · 2024Article
- Angiotensin II acts through Rac1 to upregulate pendrin: role of NADPH oxidase.American journal of physiology. Renal physiology · 2024Article
- Kidney collecting duct cells make vasopressin in response to NaCl-induced hypertonicity.JCI insight · 2022Article
- Rac1 deficiency impairs postnatal development of the renal papilla.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
A polarized collecting duct (CD), formed from the branching ureteric bud (UB), is a prerequisite for an intact kidney. The small Rho GTPase Rac1 is critical for actin cytoskeletal regulation. We investigated the role of Rac1 in the kidney collecting system by selectively deleting it in mice at the initiation of UB development. The mice exhibited only a mild developmental phenotype; however, with aging, the CD developed a disruption of epithelial integrity and function. Despite intact integrin signaling, Rac1-null CD cells had profound adhesion and polarity abnormalities that were independent of the major downstream Rac1 effector, Pak1. These cells did however have a defect in the WAVE2-Arp2/3 actin nucleation and polymerization apparatus, resulting in actomyosin hyperactivity. The epithelial defects were reversible with direct myosin II inhibition. Furthermore, Rac1 controlled lateral membrane height and overall epithelial morphology by maintaining lateral F-actin and restricting actomyosin. Thus, Rac1 promotes CD epithelial integrity and morphology by restricting actomyosin via Arp2/3-dependent cytoskeletal branching.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.