Evidence map›Paper›PMID 31226201›Full record

ArticleNucleic acids research2019

Quantitative proteomics revealed C6orf203/MTRES1 as a factor preventing stress-induced transcription deficiency in human mitochondria.

Anna V Kotrys, Dominik Cysewski, Sylwia D Czarnomska, Zbigniew Pietras, Lukasz S Borowski, Andrzej Dziembowski, Roman J Szczesny

Abstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

  1. Review
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  10. Review
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  12. Human Mitochondrial RNA Processing and Modifications: Overview.International journal of molecular sciences · 2021
    Review
  13. Article
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  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Anna V KotrysInstitute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw 02-106, Poland.
Dominik CysewskiInstitute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw 02-106, Poland.
Sylwia D CzarnomskaInstitute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw 02-106, Poland.
Zbigniew PietrasInstitute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw 02-106, Poland.
Lukasz S BorowskiInstitute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw 02-106, Poland.
Andrzej DziembowskiInstitute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw 02-106, Poland.
Roman J SzczesnyInstitute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw 02-106, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maintenance 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.

Indexed as

Gene Expression ProfilingAmino Acid SequenceGenes, MitochondrialHEK293 CellsHeLa CellsHumansMitochondriaMitochondrial ProteinsProteomeProteomicsRNA-Binding ProteinsRNA, MitochondrialSequence Homology, Amino AcidStress, PhysiologicalTranscription, GeneticMitochondrial ProteinsMTRES1 protein, humanProteomeRNA-Binding ProteinsRNA, Mitochondrial

Identifiers

PMID31226201
PMCPMC6698753

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.