Epigenetic regulator MOF drives mitochondrial metabolism

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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, th

e 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.The intricate control of cellular metabolism relies on the coordinated and harmonious interplay between the nucleus and mitochondria.

In previous studies, Asifa Akhtar's lab was able to detect MOF and several of its protein partners in mitochondria. However, the precise impact of MOF's enzymatic activity on mitochondrial function and cellular metabolism remained unknown.

Scientists have identified a protein in fruit flies that can be targeted to reverse the effects of disease-causing mutations in mitochondrial genes. The discovery could provide clues about how to ...

 

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Epigenetic regulator MOF drives mitochondrial metabolism, new study showsThe intricate control of cellular metabolism relies on the coordinated and harmonious interplay between the nucleus and mitochondria. On the one hand, mitochondria are the hub for the production of essential metabolites, which aside from being required to meet the energy demands of the cell, also serve as the building blocks for constructing both genetic and epigenetic landscapes in the nucleus. On the other hand, the majority of mitochondrial metabolic enzymes are encoded by the nuclear genome,
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