Article open access publication

Intact colonic KCa1.1 channel activity in KCNMB2 knockout mice

Physiological Reports, Wiley, ISSN 2051-817X

Volume 5, 5, 2017

DOI:10.14814/phy2.13179, Dimensions: pub.1084318961, PMC: PMC5350182, PMID: 28292889,



  1. (1) Aarhus University, grid.7048.b, AU






Mammalian potassium homeostasis results from tightly regulated renal and colonic excretion, which balances the unregulated dietary K+ intake. Colonic K+ secretion follows the pump-leak model, in which the large conductance Ca2+-activated K+ channel (KCa1.1) is well established as the sole, but highly regulated apical K+ conductance. The physiological importance of auxiliary β and γ subunits of the pore-forming α-subunit of the KCa1.1 channel is not yet fully established. This study investigates colonic K+ secretion in a global knockout mouse of the KCa1.1-β2-subunit (KCNMB2-/-), which apparently is the only β-subunit of the colonic enterocyte KCa1.1 channel. We can report that: (1) Neither KCa1.1 α- nor the remaining β-subunits were compensatory transcriptional regulated in colonic epithelia of KCNMB2-/- mice. (2) Colonic epithelia from KCNMB2-/- mice displayed equal basal and ATP-induced KCa1.1-mediated K+ conductance as compared to KCNMB2+/+ (3) K+ secretion was increased in KCNMB2-/- epithelia compared to wild-type epithelia from animals fed an aldosterone-inducing diet. (4) Importantly, the apical K+ conductance was abolished by the specific blocker of KCa1.1 channel iberiotoxin in both KCNMB2+/+ and KCNMB2-/- mice. Recently a novel family of auxiliary γ-subunits of the KCa1.1 channel has been described. (5) We detected the γ1-subunit (LRRC26) mRNA in colonic epithelia. To investigate the physiological role of the γ1-subunit of KCa1.1 channels in colonic K+ secretion, we acquired an LRRC26 knockout mouse. (6) Unexpectedly, LRRC26 mice had a perinatal lethal phenotype, thus preventing functional measurements. On this basis we conclude that colonic K+ secretion is intact or even increased in mice lacking the β2-subunit of KCa1.1 channel complex despite no additional compensatory induction of KCa1.1 β-subunits.


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