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

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 and Didier Y. R. Stainier ()
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Wenguang Yin: Max Planck Institute for Heart and Lung Research
Hyun-Taek Kim: Max Planck Institute for Heart and Lung Research
ShengPeng Wang: Max Planck Institute for Heart and Lung Research
Felix Gunawan: Max Planck Institute for Heart and Lung Research
Lei Wang: Max Planck Institute for Heart and Lung Research
Keishi Kishimoto: RIKEN Center for Developmental Biology
Hua Zhong: Baylor College of Medicine
Dany Roman: Baylor College of Medicine
Jens Preussner: ECCPS Bioinformatics and Deep Sequencing Platform
Stefan Guenther: ECCPS Bioinformatics and Deep Sequencing Platform
Viola Graef: Max Planck Institute for Heart and Lung Research
Carmen Buettner: Max Planck Institute for Heart and Lung Research
Beate Grohmann: Max Planck Institute for Heart and Lung Research
Mario Looso: ECCPS Bioinformatics and Deep Sequencing Platform
Mitsuru Morimoto: RIKEN Center for Developmental Biology
Graeme Mardon: Baylor College of Medicine
Stefan Offermanns: Max Planck Institute for Heart and Lung Research
Didier Y. R. Stainier: Max Planck Institute for Heart and Lung Research

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract 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 insight into the role of ion homeostasis in cytoskeletal organization during tubulogenesis.

Date: 2018
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DOI: 10.1038/s41467-018-05043-5

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