Petr Sergiev and Olga Dontsova have co-authored a paper “Mitochondrial rRNA Methylation by Mettl15 Contributes to the Exercise and Learning Capability in Mice” that has been recently published in International Journal of Molecular Sciences. The researchers report a study of mice devoid of Mettl15 mitochondrial 12S rRNA methyltransferase. They show that 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. They also observed accumulation of the RbfA factor, normally associated with the precursor of the 28S subunit, in the 55S mitochondrial ribosome fraction of knockout mice. The scientists find that a lack of Mettl15 leads to a lower blood glucose level after physical exercise relative to that of the wild-type mice. Moreover, they detect decreased learning capabilities in the Mettl15−/− knockout mice in the tests with both positive and negative reinforcement. Such properties make Mettl15−/− knockout mice a suitable model for mild mitochondriopathies. Full text of the paper is available here.