KCNJ15/Kir4.2 couples with polyamines to sense weak extracellular electric fields in galvanotaxis

Ken-ichi Nakajima, Kan Zhu, Yao-Hui Sun, Bence Hegyi, Qunli Zeng, Christopher J. Murphy, J. Victor Small, Ye Chen-Izu, Yoshihiro Izumiya, Josef M. Penninger () and Min Zhao ()
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Ken-ichi Nakajima: Institute for Regenerative Cures, School of Medicine, University of California Davis
Kan Zhu: Institute for Regenerative Cures, School of Medicine, University of California Davis
Yao-Hui Sun: Institute for Regenerative Cures, School of Medicine, University of California Davis
Bence Hegyi: University of California Davis
Qunli Zeng: Bioelectromagnetics Laboratory, Zhejiang University School of Medicine
Christopher J. Murphy: School of Veterinary Medicine, University of California Davis
J. Victor Small: IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences
Ye Chen-Izu: University of California Davis
Yoshihiro Izumiya: Institute for Regenerative Cures, School of Medicine, University of California Davis
Josef M. Penninger: IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences
Min Zhao: Institute for Regenerative Cures, School of Medicine, University of California Davis

Nature Communications, 2015, vol. 6, issue 1, 1-10

Abstract: Abstract Weak electric fields guide cell migration, known as galvanotaxis/electrotaxis. The sensor(s) cells use to detect the fields remain elusive. Here we perform a large-scale screen using an RNAi library targeting ion transporters in human cells. We identify 18 genes that show either defective or increased galvanotaxis after knockdown. Knockdown of the KCNJ15 gene (encoding inwardly rectifying K+ channel Kir4.2) specifically abolishes galvanotaxis, without affecting basal motility and directional migration in a monolayer scratch assay. Depletion of cytoplasmic polyamines, highly positively charged small molecules that regulate Kir4.2 function, completely inhibits galvanotaxis, whereas increase of intracellular polyamines enhances galvanotaxis in a Kir4.2-dependent manner. Expression of a polyamine-binding defective mutant of KCNJ15 significantly decreases galvanotaxis. Knockdown or inhibition of KCNJ15 prevents phosphatidylinositol 3,4,5-triphosphate (PIP3) from distributing to the leading edge. Taken together these data suggest a previously unknown two-molecule sensing mechanism in which KCNJ15/Kir4.2 couples with polyamines in sensing weak electric fields.

Date: 2015
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DOI: 10.1038/ncomms9532

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