Joiner et al. reply

Mei Ling A. Joiner; Olha M. Koval; Jingdong Li; B. Julie He; Chantal Allamargot; Zhan Gao; Elizabeth D. Luczak; Duane D. Hall; Brian D. Fink; Biyi Chen; Jinying Yang; Steven A. Moore; Thomas D. Scholz; Stefan Strack; Peter J. Mohler; William I. Sivitz; Long Sheng Song; Mark E. Anderson

doi:10.1038/nature13627

Joiner et al. reply

Mei Ling A. Joiner, Olha M. Koval, Jingdong Li, B. Julie He, Chantal Allamargot, Zhan Gao, Elizabeth D. Luczak, Duane D. Hall, Brian D. Fink, Biyi Chen, Jinying Yang, Steven A. Moore, Thomas D. Scholz, Stefan Strack, Peter J. Mohler, William I. Sivitz, Long Sheng Song, Mark E. Anderson

School of Medicine

Research output: Contribution to journal › Article › peer-review

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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.

Original language	English (US)
Pages (from-to)	E3
Journal	Nature
Volume	513
Issue number	7519
DOIs	https://doi.org/10.1038/nature13627
State	Published - Sep 25 2014

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title = "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.",

author = "Joiner, {Mei Ling A.} and Koval, {Olha M.} and Jingdong Li and He, {B. Julie} and Chantal Allamargot and Zhan Gao and Luczak, {Elizabeth D.} and Hall, {Duane D.} and Fink, {Brian D.} and Biyi Chen and Jinying Yang and Moore, {Steven A.} and Scholz, {Thomas D.} and Stefan Strack and Mohler, {Peter J.} and Sivitz, {William I.} and Song, {Long Sheng} and Anderson, {Mark E.}",

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AU - Joiner, Mei Ling A.

AU - Koval, Olha M.

AU - Li, Jingdong

AU - He, B. Julie

AU - Allamargot, Chantal

AU - Gao, Zhan

AU - Luczak, Elizabeth D.

AU - Hall, Duane D.

AU - Fink, Brian D.

AU - Chen, Biyi

AU - Yang, Jinying

AU - Moore, Steven A.

AU - Scholz, Thomas D.

AU - Strack, Stefan

AU - Mohler, Peter J.

AU - Sivitz, William I.

AU - Song, Long Sheng

AU - Anderson, Mark E.

PY - 2014/9/25

Y1 - 2014/9/25

N2 - 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.

AB - 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.

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Joiner et al. reply

Abstract

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