Evidence map›Paper›PMID 20004207›Full record

ArticleJournal of molecular biology2010

Combination of the loss of cmnm5U34 with the lack of s2U34 modifications of tRNALys, tRNAGlu, and tRNAGln altered mitochondrial biogenesis and respiration.

Xinjian Wang, Qingfeng Yan, Min-Xin Guan

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
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

31 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. The first apicoplast tRNA thiouridylase plays a vital role in the growth ofFrontiers in cellular and infection microbiology · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Naturally occurring modified ribonucleosides.Wiley interdisciplinary reviews. RNA · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. The genotypic and phenotypic spectrum of MTO1 deficiency.Molecular genetics and metabolism · 2018
    Article
  17. Article
  18. Review
  19. Article
  20. 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

3 authors at 2 institutions in 2 countries.

Xinjian WangDivision of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Qingfeng Yan
Min-Xin Guan
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati Medical Center · US

Funding

Molecular Mechanism of Aminoglycoside OtotoxicityR01DC005230 · NIDCD · CINCINNATI CHILDRENS HOSP MED CTR · PI GUAN, MIN-XIN · 2002 to 2006
$1.8M
Nuclear modifier genes for maternally inherited deafnessR01DC007696 · NIDCD · CINCINNATI CHILDRENS HOSP MED CTR · PI GUAN, MIN-XIN · 2007 to 2010
$1.3M
NIDCD NIH HHS R01 DC005230NIDCD NIH HHS R01 DC007696NIDCD NIH HHS R01DC05230NIDCD NIH HHS R01DC07696
6 · The paper itself

Abstract

Yeast Saccharomyces cerevisiae MTO2, MTO1, and MSS1 genes encoded highly conserved tRNA modifying enzymes for the biosynthesis of carboxymethylaminomethyl (cmnm)(5)s(2)U(34) in mitochondrial tRNA(Lys), tRNA(Glu), and tRNA(Gln). In fact, Mto1p and Mss1p are involved in the biosynthesis of the cmnm(5) group (cmnm(5)U(34)), while Mto2p is responsible for the 2-thiouridylation (s(2)U(34)) of these tRNAs. Previous studies showed that partial modifications at U(34) in mitochondrial tRNA enabled mto1, mto2, and mss1 strains to respire. In this report, we investigated the functional interaction between MTO2, MTO1, and MSS1 genes by using the mto2, mto1, and mss1 single, double, and triple mutants. Strikingly, the deletion of MTO2 was synthetically lethal with a mutation of MSS1 or deletion of MTO1 on medium containing glycerol but not on medium containing glucose. Interestingly, there were no detectable levels of nine tRNAs including tRNA(Lys), tRNA(Glu), and tRNA(Gln) in mto2/mss1, mto2/mto1, and mto2/mto1/mss1 strains. Furthermore, mto2/mss1, mto2/mto1, and mto2/mto1/mss1 mutants exhibited extremely low levels of COX1 and CYTB mRNA and 15S and 21S rRNA as well as the complete loss of mitochondrial protein synthesis. The synthetic enhancement combinations likely resulted from the completely abolished modification at U(34) of tRNA(Lys), tRNA(Glu), and tRNA(Gln), caused by the combination of eliminating the 2-thiouridylation by the mto2 mutation with the absence of the cmnm(5)U(34) by the mto1 or mss1 mutation. The complete loss of modifications at U(34) of tRNAs altered mitochondrial RNA metabolisms, causing a degradation of mitochondrial tRNA, mRNA, and rRNAs. As a result, failures in mitochondrial RNA metabolisms were responsible for the complete loss of mitochondrial translation. Consequently, defects in mitochondrial protein synthesis caused the instability of their mitochondrial genomes, thus producing the respiratory-deficient phenotypes. Therefore, our findings demonstrated a critical role of modifications at U(34) of tRNA(Lys), tRNA(Glu), and tRNA(Gln) in maintenance of mitochondrial genome, mitochondrial RNA stability, translation, and respiratory function.

Indexed as

AllelesBase SequenceGenes, FungalGenome, MitochondrialGTP-Binding ProteinsMitochondriaMitochondrial ProteinsMutationOxygen ConsumptionPhenotypeRNARNA-Binding ProteinsRNA, FungalRNA, MitochondrialRNA, Transfer, GlnRNA, Transfer, GluGTP-Binding ProteinsMitochondrial ProteinsMSS1 protein, S cerevisiaeMTO1 protein, S cerevisiaeRNARNA-Binding ProteinsRNA, FungalRNA, MitochondrialRNA, Transfer, GlnRNA, Transfer, GluRNA, Transfer, LysSaccharomyces cerevisiae Proteins

Identifiers

PMID20004207
PMCPMC2818684
OpenAlexW2074400862

What OpenQuestion holds

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Registered trials

None linked

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.