Regulation of mitochondrial gene expression in Saccharomyces cerevisiae: the role of RNA-binding enzymes

2001 ◽  
Vol 1 (S1) ◽  
Author(s):  
H van der Spek ◽  
M Siep ◽  
L de Jong ◽  
SDJ Elzinga ◽  
K van Oosterum ◽  
...  
2019 ◽  
Vol 47 (14) ◽  
pp. 7502-7517 ◽  
Author(s):  
Anna V Kotrys ◽  
Dominik Cysewski ◽  
Sylwia D Czarnomska ◽  
Zbigniew Pietras ◽  
Lukasz S Borowski ◽  
...  

AbstractMaintenance of mitochondrial gene expression is crucial for cellular homeostasis. Stress conditions may lead to a temporary reduction of mitochondrial genome copy number, raising the risk of insufficient expression of mitochondrial encoded genes. Little is known how compensatory mechanisms operate to maintain proper mitochondrial transcripts levels upon disturbed transcription and which proteins are involved in them. Here we performed a quantitative proteomic screen to search for proteins that sustain expression of mtDNA under stress conditions. Analysis of stress-induced changes of the human mitochondrial proteome led to the identification of several proteins with poorly defined functions among which we focused on C6orf203, which we named MTRES1 (Mitochondrial Transcription Rescue Factor 1). We found that the level of MTRES1 is elevated in cells under stress and we show that this upregulation of MTRES1 prevents mitochondrial transcript loss under perturbed mitochondrial gene expression. This protective effect depends on the RNA binding activity of MTRES1. Functional analysis revealed that MTRES1 associates with mitochondrial RNA polymerase POLRMT and acts by increasing mitochondrial transcription, without changing the stability of mitochondrial RNAs. We propose that MTRES1 is an example of a protein that protects the cell from mitochondrial RNA loss during stress.


Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 757-760 ◽  
Author(s):  
Ronald A. Butow ◽  
Hong Zhu ◽  
Philip Perlman ◽  
Heather Conrad-Webb

All mRNAs on the yeast mitochondrial genome terminate at a conserved dodecamer sequence 5′-AAUAAUAUUCUU-3′. We have characterized two mutants with altered dodecamers. One contains a deletion of the dodecamer at the end of the var1 gene, and the other contains two adjacent transversions in the dodecamer at the end of the reading frame of fit1, a gene within the ω+ allele of the 21S rRNA gene. In each mutant, expression of the respective gene is blocked completely. A dominant nuclear suppressor, SUV3-1, was isolated that suppresses the var1 deletion but is without effect on the fit1 dodecamer mutations. Unexpectedly, however, we found that SUV3-1 blocks expression of the wild-type fit1 allele by blocking processing at its dodecamer. SUV3-1 has pleiotropic effects on mitochondrial gene expression, affecting RNA processing, RNA stability, and translation. Our results suggest that RNA metabolism and translation may be part of a multicomponent complex within mitochondria.Key words: mitochondria, yeast, mRNA, RNA processing, 3′ dodecamer.


2006 ◽  
Vol 12 (8) ◽  
pp. S162-S163
Author(s):  
Yasuaki Nakagawa ◽  
Koichiro Kuwahara ◽  
Masaki Harada ◽  
Genzo Takemura ◽  
Masaharu Akao ◽  
...  

2001 ◽  
Vol 54 ◽  
pp. S11-S27 ◽  
Author(s):  
Carolyn D Berdanier ◽  
Helen B Everts ◽  
Christina Hermoyian ◽  
Clayton E Mathews

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