PubMed · 14802941
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A FLEISCH. 1950. [Double coupled spirometer].. https://pubmed.ncbi.nlm.nih.gov/14802941/
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Mitochondria have a single release factor that recognizes all stop codons in mRNAs. The yeast mitochondrial release factor, mRF1, is a protein of 43 kDa that emerges from its precursor by cleavage of a mitochondrial targeting sequence. mRF1 is localized exclusively in mitochondria, even when it is overproduced. A several-fold increase in mRF1 levels slightly inhibits the growth of wild-type cells on media containing a non-fermentable carbon source. A direct antisuppressor effect of overproduced mRF1 is observed, since the MRF1 gene on a multicopy plasmid causes Gly(-) phenotypes of the leaky mit(-) point mutations in mtDNA. We also examine steady-state mRF1 levels in a respiratory-deficient mrf1-780 mutant with inhibited mitochondrial translation. We show that both the mRF1 protein and the MRF1 transcript are elevated in mrf1-780 cells. A similar increase in mRF1 expression is observed in the rho(0) strain with no mitochondrial translation. This is indicative of retrograde signalling in the regulation of MRF1 expression. According to our hypothesis, inhibition of translation in the mrf1-780 strain is due to mitoribosome stalling at the stop codon and the observed elevated level of release factor is a secondary effect of respiratory deficiency.
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Investigations on the mechanisms capable of influencing heart mitochondrial function constitute a central contribution to the understanding of cardiac bioenergetics. In contrast to the conventional idea that reactive oxygen species (ROS) mostly act as a trigger for oxidative damage of biological structures, in low physiological concentrations they can regulate a variety of important molecular mechanisms, including those related to mitochondrial respiratory function. Among others, moderate physical exercise seems to be an important agent to induce cellular and mitochondrial environmental redox modifications and it is possible that these alterations could mediate cardiac mitochondrial respiration patterns. This brief review summarizes some current knowledge on mitochondrial respiratory pathways and focuses on data provided by studies dealing with exercise and cardiac respiratory mechanisms. It is emphasized the need of further experimental studies that analyze the association between physical exercise, particularly endurance training, and several mechanisms hypothetically related to the improvement of mitochondrial function, such as the overexpression of some important chaperone machinery and the up-regulation of both cellular and mitochondrial antioxidants. The influence of chronic moderate exercise on the functionality of some inner membrane components and on mitochondrial calcium loading capacity remains to be established.