PubMed · 14095924
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S A KLEIN. 1963-11-28. [RESUSCITATION].. https://pubmed.ncbi.nlm.nih.gov/14095924/
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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.
In isolated potato tuber mitochondria, palmitic acid (PA) can induce a H+ leak inhibited by GTP in the phosphorylating (state 3) respiration but not in the resting (state 4) respiration. The PA-induced H+ leak is constant when state 3 respiration is decreased by an inhibition of the succinate uptake with n-butyl malonate (nBM). We show that the efficiency of inhibition by GTP is decreased when state 3 respiration is progressively inhibited by antimycin A (AA) and is restored following subsequent addition of nBM. We propose that in phosphorylating potato tuber mitochondria, the redox state of ubiquinone, which can antagonistically be varied with AA and nBM, modulates inhibition of the PA-activated UCP-sustained H+ leak by GTP.
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