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The  Chchd10  gene encodes a coiled-coil-helix-coiled-coil-helix-domain containing protein predicted to function in the mitochondrion and nucleus. Mutations of  Chchd10  are associated with ALS, dementia and myopathy in humans and animal models, but how knockout of  Chchd10  ( Chchd10   KO  ) affects various tissues especially skeletal muscle and adipose tissues remains unclear. Here we show that  Chchd10  expression increases as myoblasts and preadipocytes differentiate. During myogenesis, CHCHD10 interacts with TAR DNA binding protein 43 (TDP-43) in regenerating myofibers in vivo and in newly differentiated myotubes ex vivo. Surprisingly,  Chchd10   KO   mice had normal skeletal muscle development, growth and regeneration, with moderate defects in grip strength and motor performance.  Chchd10   KO   similarly had no effects on development of brown and white adipose tissues (WAT). However,  Chchd10   KO   mice had blunted response to acute cold and attenuated cold-induced browning of WAT, with markedly reduced UCP1 levels. Together, these results demonstrate that  Chchd10  is dispensable for normal myogenesis and adipogenesis but is required for normal motility and cold-induced, mitochondrion-dependent browning of adipocytes. The data also suggest that human  CHCHD10  mutations cause myopathy through a gain-of-function mechanism.

Chchd10 is dispensable for myogenesis but critical for adipose browning