Researchers have unveiled a new mechanism for regulating mitochondrial function. The findings reveal the critical role played by the enzymatic activity of the lysine acetyltransferase MOF in maintaining mitochondrial integrity and function through acetylation of mitochondrial electron transport chain component COX17. Cells lacking MOF-mediated COX17 acetylation exhibit dramatic mitochondrial defects and impaired ability to produce energy. Underscoring the clinical relevance of these findings, the team also showed that cells from human patients with a developmental disorder caused by mutations in MOF also exhibited respiratory defects that could be ameliorated by interventions such as acetylation-mimetic COX17 or mitochondrially targeted MOF.
Epigenetic regulator MOF drives mitochondrial metabolism
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