scholarly journals S. cerevisiae Strain Lacking Mitochondrial IF3 Shows Increased Levels of Tma19p during Adaptation to Respiratory Growth

Cells ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 645 ◽  
Author(s):  
Levitskii ◽  
Baleva ◽  
Chicherin ◽  
Krasheninnikov ◽  
Kamenski

After billions of years of evolution, mitochondrion retains its own genome, which gets expressed in mitochondrial matrix. Mitochondrial translation machinery rather differs from modern bacterial and eukaryotic cytosolic systems. Any disturbance in mitochondrial translation drastically impairs mitochondrial function. In budding yeast Saccharomyces cerevisiae, deletion of the gene coding for mitochondrial translation initiation factor 3 - AIM23, leads to an imbalance in mitochondrial protein synthesis and significantly delays growth after shifting from fermentable to non-fermentable carbon sources. Molecular mechanism underlying this adaptation to respiratory growth was unknown. Here, we demonstrate that slow adaptation from glycolysis to respiration in the absence of Aim23p is accompanied by a gradual increase of cytochrome c oxidase activity and by increased levels of Tma19p protein, which protects mitochondria from oxidative stress.

2020 ◽  
Vol 21 (10) ◽  
pp. 3414
Author(s):  
Ivan Chicherin ◽  
Sergey Levitskii ◽  
Maria V. Baleva ◽  
Igor A. Krasheninnikov ◽  
Maxim V. Patrushev ◽  
...  

Mitochondrial genomes code for several core components of respiratory chain complexes. Thus, mitochondrial translation is of great importance for the organelle as well as for the whole cell. In yeast, mitochondrial translation initiation factor 3, Aim23p, is not essential for the organellar protein synthesis; however, its absence leads to a significant quantitative imbalance of the mitochondrial translation products. This fact points to a possible specific action of Aim23p on the biosynthesis of some mitochondrial protein species. In this work, we examined such peculiar effects of Aim23p in relation to yeast mitochondrial COX2 mRNA translation. We show that Aim23p is indispensable to this process. According to our data, this is mediated by Aimp23p interaction with the known specific factor of the COX2 mRNA translation, Pet111p. If there is no Aim23p in the yeast cells, an increased amount of Pet111p ensures proper COX2 mRNA translation. Our results demonstrate the additional non-canonical function of initiation factor 3 in yeast mitochondrial translation.


2010 ◽  
Vol 486 (3) ◽  
pp. 228-230 ◽  
Author(s):  
Bahareh Behrouz ◽  
Carles Vilariño-Güell ◽  
Michael G. Heckman ◽  
Alexandra I. Soto-Ortolaza ◽  
Jan O. Aasly ◽  
...  

2014 ◽  
Vol 306 (5) ◽  
pp. E503-E511 ◽  
Author(s):  
Nicholas P. Greene ◽  
Mats I. Nilsson ◽  
Tyrone A. Washington ◽  
David E. Lee ◽  
Lemuel A. Brown ◽  
...  

Previously, we demonstrated that high-volume resistance exercise stimulates mitochondrial protein synthesis (a measure of mitochondrial biogenesis) in lean but not obese Zucker rats. Here, we examined factors involved in regulating mitochondrial biogenesis in the same animals. PGC-1α was 45% higher following exercise in obese but not lean animals compared with sedentary counterparts. Interestingly, exercised animals demonstrated greater PPARδ protein in both lean (47%) and obese (>200%) animals. AMPK phosphorylation (300%) and CPT-I protein (30%) were elevated by exercise in lean animals only, indicating improved substrate availability/flux. These findings suggest that, despite PGC-1α induction, obese animals were resistant to exercise-induced synthesis of new mitochondrial and oxidative protein. Previously, we reported that most anabolic processes are upregulated in these same obese animals regardless of exercise, so the purpose of this study was to assess specific factors associated with the mitochondrial genome as possible culprits for impaired mitochondrial biogenesis. Exercise resulted in higher mRNA contents of mitochondrial transcription factor A (∼50% in each phenotype) and mitochondrial translation initiation factor 2 (31 and 47% in lean and obese, respectively). However, mitochondrial translation elongation factor-Tu mRNA was higher following exercise in lean animals only (40%), suggesting aberrant regulation of mitochondrial translation elongation as a possible culprit in impaired mitochondrial biogenesis following exercise with obesity.


iScience ◽  
2019 ◽  
Vol 12 ◽  
pp. 76-86 ◽  
Author(s):  
Ravi K. Koripella ◽  
Manjuli R. Sharma ◽  
Md. Emdadul Haque ◽  
Paul Risteff ◽  
Linda L. Spremulli ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
Anna Anvret ◽  
Caroline Ran ◽  
Marie Westerlund ◽  
Ann-Christin Thelander ◽  
Olof Sydow ◽  
...  

Genes important for mitochondrial function have been implicated in Parkinson's disease (PD). Mitochondrial translation initiation factor 3 (MTIF3) is a nuclear encoded protein required for the initiation of complex formation on mitochondrial ribosomes. Dysfunction of MTIF3 may impair mitochondrial function and dopamine neurons appear to be particularly vulnerable to oxidative stress, which may relate to their degeneration in PD. An association was recently reported between the synonymous rs7669(C>T) in MTIF3 and PD in a German case-control material. We investigated rs7669 in a Swedish Parkinson case-control material. The study revealed no significant association of the individual genotypes or alleles with PD. When comparing the combined TT/CT-genotypes versus the CC-genotype, we observed a significant association (P=.0473) with PD. We also demonstrated that the TT-genotype causes a significant decrease in MTIF3 mRNA expression compared to the CC-genotype (P=.0163). Our findings support the hypothesis that MTIF3 may be involved in the etiology of PD.


2014 ◽  
Vol 34 (6) ◽  
pp. 1046-1053 ◽  
Author(s):  
Y. Martineau ◽  
X. Wang ◽  
T. Alain ◽  
E. Petroulakis ◽  
D. Shahbazian ◽  
...  

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