Rac1 restrains actomyosin to enable ciliogenesis and mechanosensing in the postnatal kidney.

Mice lacking Rac1 in the developing nephron die within weeks of birth from multicystic dysplastic kidney, showing Rac1 is essential for postnatal kidney maturation.

• Why it matters: Familial CAKUT variants implicate altered Rho GTPase signaling in MCDK, but how Rac1 shapes postnatal differentiation and mechanosensing in the kidney was unclear.
• What they did: The study used Rac1-deficient mice to test whether Rac1 coordinates actomyosin regulation, primary cilia formation, and fluid shear stress sensing, including GEF-H1-dependent contractility and pharmacologic myosin inhibition.
• The result: Rac1 restrains GEF-H1-dependent actomyosin contractility to enable apical actin clearing and ciliogenesis; myosin inhibition restored ciliogenesis and flow-induced differentiation in cells and attenuated cystic-dysplastic remodeling in Rac1 mutant mice.

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