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Nat Commun. 2018 Jul 19;9(1):2815. doi: 10.1038/s41467-018-05043-5.

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

Author information

1
Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany. Wenguang.Yin@mpi-bn.mpg.de.
2
Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.
3
Department of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.
4
Cardiovascular Research Center, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, 710061, China.
5
Laboratory for Lung Development, RIKEN Center for Developmental Biology, Kobe, 650-0047, Japan.
6
Departments of Pathology and Immunology and Molecular and Human Genetics, Integrative Molecular and Biomedical Sciences Program, Baylor College of Medicine, Houston, TX, 77030, USA.
7
Max Planck Institute for Heart and Lung Research, ECCPS Bioinformatics and Deep Sequencing Platform, Bad Nauheim, 61231, Germany.
8
Center for Molecular Medicine, Goethe University, Frankfurt, 60590, Germany.
9
Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany. Didier.Stainier@mpi-bn.mpg.de.

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.

PMID:
30022023
PMCID:
PMC6052067
DOI:
10.1038/s41467-018-05043-5
[Indexed for MEDLINE]
Free PMC Article

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