KCNE1 divides the voltage sensor movement in KCNQ1/KCNE1 channels into two steps

Rene Barro-Soria, Santiago Rebolledo, Sara I. Liin, Marta E. Perez, Kevin J. Sampson, Robert S. Kass and H. Peter Larsson ()
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Rene Barro-Soria: Miller School of Medicine, University of Miami
Santiago Rebolledo: Miller School of Medicine, University of Miami
Sara I. Liin: Miller School of Medicine, University of Miami
Marta E. Perez: Miller School of Medicine, University of Miami
Kevin J. Sampson: College of Physicians and Surgeons of Columbia University
Robert S. Kass: College of Physicians and Surgeons of Columbia University
H. Peter Larsson: Miller School of Medicine, University of Miami

Nature Communications, 2014, vol. 5, issue 1, 1-12

Abstract: Abstract The functional properties of KCNQ1 channels are highly dependent on associated KCNE-β subunits. Mutations in KCNQ1 or KCNE subunits can cause congenital channelopathies, such as deafness, cardiac arrhythmias and epilepsy. The mechanism by which KCNE1-β subunits slow the kinetics of KCNQ1 channels is a matter of current controversy. Here we show that KCNQ1/KCNE1 channel activation occurs in two steps: first, mutually independent voltage sensor movements in the four KCNQ1 subunits generate the main gating charge movement and underlie the initial delay in the activation time course of KCNQ1/KCNE1 currents. Second, a slower and concerted conformational change of all four voltage sensors and the gate, which opens the KCNQ1/KCNE1 channel. Our data show that KCNE1 divides the voltage sensor movement into two steps with widely different voltage dependences and kinetics. The two voltage sensor steps in KCNQ1/KCNE1 channels can be pharmacologically isolated and further separated by a disease-causing mutation.

Date: 2014
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DOI: 10.1038/ncomms4750

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