Joiner et al. reply

Abstract

Replying to F. Fieni et al. 513, http://dx.doi.org/10.1038/nature13626 (2014)In our Letter identifying mitochondrial CaMKII as a crucial component of a Ca 2+ -dependent process of heart disease, we used multiple methods to show that CaMKII modulates mitochondrial Ca 2+ homeostasis, as outlined below. First, we carried out electrophysiology of the mitochondrial calcium uniporter (MCU) current in mitoplasts. In our report we did not claim to measure capacitance of the mitoplast separately from the total capacitance of the mitoplast and pipette. Although we concede that the approach of Fieni et al. is preferable, we found that even after removing any correction for capacitance, dialysis with constitutively active CaMKII monomers increased MCU current whereas dialysis with catalytically dead CaMKII monomers did not.