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The potassium channel KCNJ13 is essential for smooth muscle cytoskeletal organization during mouse tracheal tubulogenesis

By Wenguang Yin, Hyun-Taek Kim, ShengPeng Wang, Felix Gunawan, Lei Wang, Keishi Kishimoto, Hua Zhong, Dany Roman, Jens Preussner, Stefan Guenther, Viola Graef, Carmen Buettner, Beate Grohmann, Mario Looso, Mitsuru Morimoto, Graeme Mardon, Stefan Offermanns, Didier Y.R. Stainier

Posted 11 May 2018
bioRxiv DOI: 10.1101/320119 (published DOI: 10.1038/s41467-018-05043-5)

Tubulogenesis is essential for the formation and function of internal organs. One such organ is the trachea, which allows gas exchange between the external environment and the lungs. However, the cellular and molecular mechanisms underlying tracheal tube development remain poorly understood. Here, we show that the potassium channel KCNJ13 is a critical modulator of tracheal tubulogenesis. We identify Kcnj13 in an ethylnitrosourea forward genetic screen for regulators of mouse respiratory organ development. Kcnj13 mutants exhibit a shorter trachea as well as defective smooth muscle (SM) cell alignment and polarity. KCNJ13 is essential to maintain ion homeostasis in tracheal SM cells, which is required for actin polymerization. This process appears to be mediated, at least in part, through activation of the actin regulator AKT, as pharmacological increase of AKT phosphorylation ameliorates the Kcnj13 mutant trachea phenotypes. These results provide insights into the role of ion homeostasis in cytoskeletal organization during tubulogenesis.

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