TY - JOUR
T1 - Control of organelle gene expression by the mitochondrial transcription termination factor mTERF22 in Arabidopsis thaliana plants
AU - Shevtsov, Sofia
AU - Nevo-Dinur, Keren
AU - Faigon, Lior
AU - Sultan, Laure D.
AU - Zmudjak, Michal
AU - Markovits, Mark
AU - Ostersetzer-Biran, Oren
N1 - Publisher Copyright:
© 2018 Shevtsov et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2018/7/1
Y1 - 2018/7/1
N2 - Mitochondria are key sites for cellular energy metabolism and are essential to cell survival. As descendants of eubacterial symbionts (specifically α-proteobacteria), mitochondria contain their own genomes (mtDNAs), RNAs and ribosomes. Plants need to coordinate their energy demands during particular growth and developmental stages. The regulation of mtDNA expression is critical for controlling the oxidative phosphorylation capacity in response to physiological or environmental signals. The mitochondrial transcription termination factor (mTERF) family has recently emerged as a central player in mitochondrial gene expression in various eukaryotes. Interestingly, the number of mTERFs has been greatly expanded in the nuclear genomes of plants, with more than 30 members in different angiosperms. The majority of the annotated mTERFs in plants are predicted to be plastid- or mitochondria-localized. These are therefore expected to play important roles in organellar gene expression in angiosperms. Yet, functions have been assigned to only a small fraction of these factors in plants. Here, we report the characterization of mTERF22 (At5g64950) which functions in the regulation of mtDNA transcription in Arabidopsis thaliana. GFP localization assays indicate that mTERF22 resides within the mitochondria. Disruption of mTERF22 function results in reduced mtRNA accumulation and altered organelle biogenesis. Transcriptomic and run-on experiments suggest that the phenotypes of mterf22 mutants are attributable, at least in part, to altered mitochondria transcription, and indicate that mTERF22 affects the expression of numerous mitochondrial genes in Arabidopsis plants.
AB - Mitochondria are key sites for cellular energy metabolism and are essential to cell survival. As descendants of eubacterial symbionts (specifically α-proteobacteria), mitochondria contain their own genomes (mtDNAs), RNAs and ribosomes. Plants need to coordinate their energy demands during particular growth and developmental stages. The regulation of mtDNA expression is critical for controlling the oxidative phosphorylation capacity in response to physiological or environmental signals. The mitochondrial transcription termination factor (mTERF) family has recently emerged as a central player in mitochondrial gene expression in various eukaryotes. Interestingly, the number of mTERFs has been greatly expanded in the nuclear genomes of plants, with more than 30 members in different angiosperms. The majority of the annotated mTERFs in plants are predicted to be plastid- or mitochondria-localized. These are therefore expected to play important roles in organellar gene expression in angiosperms. Yet, functions have been assigned to only a small fraction of these factors in plants. Here, we report the characterization of mTERF22 (At5g64950) which functions in the regulation of mtDNA transcription in Arabidopsis thaliana. GFP localization assays indicate that mTERF22 resides within the mitochondria. Disruption of mTERF22 function results in reduced mtRNA accumulation and altered organelle biogenesis. Transcriptomic and run-on experiments suggest that the phenotypes of mterf22 mutants are attributable, at least in part, to altered mitochondria transcription, and indicate that mTERF22 affects the expression of numerous mitochondrial genes in Arabidopsis plants.
UR - http://www.scopus.com/inward/record.url?scp=85050821717&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0201631
DO - 10.1371/journal.pone.0201631
M3 - Article
C2 - 30059532
AN - SCOPUS:85050821717
SN - 1932-6203
VL - 13
JO - PLoS ONE
JF - PLoS ONE
IS - 7
M1 - e0201631
ER -