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. 2024 Apr 30;121(19):e2317753121. doi: 10.1073/pnas.2317753121

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Copyright © 2024 the Author(s). Published by PNAS.

This open access article is distributed under Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND).

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Fig. 2. — SLO-2 is activated by external calcium and by VICR. (A–D) Ik_hiCl was significantly decreased by a general CaV pore blocker (Cd²⁺) and in recordings lacking external calcium. Ik_hiCl currents were recorded from adult body wall muscles at holding potentials of −60 to +60 mV. Representative Ik_hiCl traces (A) and mean current density at +30 mV (B and D) are shown. The inhibitory effect of Cd²⁺ on Ik_hiCl was eliminated in slo-2 mutants (B), suggesting that SLO-2 mediates the Cd²⁺ sensitive K current. Ik_hiCl recorded in 5 mM and 0 external Ca²⁺ were not significantly different from slo-2 mutants (D), demonstrating that SLO-2 mediates the K current activated by external calcium. (C and D) CPA treatment reduced the Ik_hiCl recorded in 0 Ca² to levels found in slo-2 mutants. These results suggest that the residual SLO-2 activation observed when external calcium entry is blocked is mediated by VICR. Representative traces (C) and mean current density at +30 mV (D) are shown. Values that differ significantly are indicated (ns, not significant; ***P < 0.001; ****P < 0.0001). Error bars indicate SEM.