Mitochondrial rRNA Methylation by Mettl15 Contributes to the Exercise and Learning Capability in Mice.

ABSTRACT: Mitochondrial translation is a unique relic of the symbiotic origin of the organelle. Alterations of its components cause a number of severe human diseases. Hereby we report a study of mice devoid of Mettl15 mitochondrial 12S rRNA methyltransferase, responsible for the formation of m⁴C839 residue (human numbering). Homozygous Mettl15^-/- mice appeared to be viable in contrast to other mitochondrial rRNA methyltransferase knockouts reported earlier. The phenotype of Mettl15^-/- mice is much milder than that of other mutants of mitochondrial translation apparatus. In agreement with the results obtained earlier for cell cultures with an inactivated Mettl15 gene, we observed accumulation of the RbfA factor, normally associated with the precur

SUBMITTER: Averina OA 

PROVIDER: S-EPMC9181494 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature