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Cell Metab. 2014 Dec 2;20(6):1069-75. doi: 10.1016/j.cmet.2014.11.005.

The respiratory chain supercomplex organization is independent of COX7a2l isoforms.

Author information

1
Department of Mitochondrial Biology, Max Planck Institute for Biology of Ageing, Joseph-Stelzmann-Strasse 9b, 50931 Cologne, Germany.
2
Department of Mitochondrial Biology, Max Planck Institute for Biology of Ageing, Joseph-Stelzmann-Strasse 9b, 50931 Cologne, Germany; Department of Laboratory Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden. Electronic address: larsson@age.mpg.de.
3
Department of Mitochondrial Biology, Max Planck Institute for Biology of Ageing, Joseph-Stelzmann-Strasse 9b, 50931 Cologne, Germany. Electronic address: dmilenkovic@age.mpg.de.

Abstract

The organization of individual respiratory chain complexes into supercomplexes or respirasomes has attracted great interest because of the implications for cellular energy conversion. Recently, it was reported that commonly used mouse strains harbor a short COX7a2l (SCAFI) gene isoform that supposedly precludes the formation of complex IV-containing supercomplexes. This claim potentially has serious implications for numerous mouse studies addressing important topics in metabolism, including adaptation to space flights. Using several complementary experimental approaches, we show that mice with the short COX7a2l isoform have normal biogenesis and steady-state levels of complex IV-containing supercomplexes and consequently have normal respiratory chain function. Furthermore, we use a mouse knockout of Lrpprc and show that loss of complex IV compromises respirasome formation. We conclude that the presence of the short COX7a2l isoform in the commonly used C57BL/6 mouse strains does not prevent their use in metabolism research.

PMID:
25470551
PMCID:
PMC4261080
DOI:
10.1016/j.cmet.2014.11.005
[Indexed for MEDLINE]
Free PMC Article

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