Mitochondrial Ca2+ uniporter and CaMKII in heart

Francesca Fieni, Derrick E. Johnson, Andy Hudmon and Yuriy Kirichok ()
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Francesca Fieni: University of California San Francisco
Derrick E. Johnson: Stark Neuroscience Research Institute, Indiana University School of Medicine
Andy Hudmon: Stark Neuroscience Research Institute, Indiana University School of Medicine
Yuriy Kirichok: University of California San Francisco

Nature, 2014, vol. 513, issue 7519, E1-E2

Abstract: Abstract Arising from M. A. Joiner et al. Nature 491, 269–273 (2012); doi:10.1038/nature1023410.1038/nature11444 The influx of cytosolic Ca2+ into mitochondria is mediated primarily by the mitochondrial calcium uniporter (MCU)1, a small-conductance, Ca2+-selective channel2,3,4,5,6—MCU modulates intracellular Ca2+ transients and regulates ATP production and cell death1. Recently, Joiner et al. reported that MCU is regulated by mitochondrial CaMKII, and this regulation determines stress response in heart7. They reported a very large current putatively mediated by MCU that was about two orders of magnitude greater than the MCU current (IMCU) that we previously measured in heart mitochondria3; furthermore, the current traces presented by Joiner et al. showed unusually high fluctuations incompatible with the low single-channel conductance of MCU. Here we performed patch-clamp recordings from mouse heart mitochondria under the exact conditions used by Joiner et al.7, and confirm that IMCU in cardiomyocytes is very small and is not directly regulated by CaMKII; thus, the currents presented by Joiner et al. do not appear to correspond to MCU, and there is no direct electrophysiological evidence that CaMKII regulates MCU. There is a Reply to this Brief Communication Arising by Joiner, M. A. et al. Nature 513, http://dx.doi.org/10.1038/nature13627 (2014).

Date: 2014
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DOI: 10.1038/nature13626

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