Evidence map›Paper›PMID 15944150›Full record

ArticleThe Journal of biological chemistry2005

Mutations in MTO2 related to tRNA modification impair mitochondrial gene expression and protein synthesis in the presence of a paromomycin resistance mutation in mitochondrial 15 S rRNA.

Qingfeng Yan, Xiaoming Li, Gèrard Faye, Min-Xin Guan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

26 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The mitogenomes of two saprophytic Boletales species (Computational and structural biotechnology journal · 2021
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Contribution of the tRNAThe Journal of biological chemistry · 2018
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
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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

4 authors at 2 institutions in 3 countries.

Qingfeng YanDivision and Program in Human Genetics and Center for Hearing and Deafness Research, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Xiaoming Li
Gèrard Faye
Min-Xin Guan
Cincinnati Children's Hospital Medical Center · USInstitut Curie · FR

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
Genetic Correction of Maternally Inherited DiseasesR01NS044015 · NINDS · CHILDREN'S HOSPITAL MED CTR (CINCINNATI) · PI GUAN, MIN-XIN · 2002 to 2004
$525k
Biochemical Basis of Maternally Inherited DeafnessR03DC004958 · NIDCD · CHILDREN'S HOSPITAL MED CTR (CINCINNATI) · PI GUAN, MIN-XIN · 2001 to 2003
$222k
NIDCD NIH HHS R01 DC005230NIDCD NIH HHS R01 DC007696NIDCD NIH HHS R01DC05230NIDCD NIH HHS R03 DC004958NINDS NIH HHS R01 NS044015NINDS NIH HHS R01NS44015
6 · The paper itself

Abstract

Nuclear gene(s) have been shown to modulate the phenotypic expression of mitochondrial DNA mutations. We report here the identification and characterization of the yeast nuclear gene MTO2 encoding an evolutionarily conserved protein involved in mitochondrial tRNA modification. Interestingly, mto2 null mutants expressed a respiratory-deficient phenotype when coexisting with the C1409G mutation of mitochondrial 15 S rRNA at the very conservative site for human deafness-associated 12 S rRNA A1491G and C1409T mutations. Furthermore, the overall rate of mitochondrial translation was markedly reduced in a yeast mto2 strain in the wild type mitochondrial background, whereas mitochondrial protein synthesis was almost abolished in a yeast mto2 strain carrying the C1409G allele. The other interesting feature of mto2 mutants is the defective expression of mitochondrial genes, especially CYTB and COX1, but only when coexisting with the C1409G allele. These data strongly indicate that a product of MTO2 functionally interacts with the decoding region of 15 S rRNA, particularly at the site of the C1409G or A1491G mutation. In addition, we showed that yeast and human Mto2p localize in mitochondria. The isolated human MTO2 cDNA can partially restore the respiratory-deficient phenotype of yeast mto2 cells carrying the C1409G mutation. These functional conservations imply that human MTO2 may act as a modifier gene, modulating the phenotypic expression of the deafness-associated A1491G or C1409T mutation in mitochondrial 12 S rRNA.

Indexed as

Gene Expression RegulationMutationAllelesBase SequenceCell NucleusDeafnessDNA, ComplementaryDrug ResistanceEscherichia coliGenotypeHumansMitochondriaMitochondrial ProteinsMolecular Sequence DataNucleic Acid ConformationParomomycinDNA, ComplementaryMitochondrial ProteinsParomomycinRNA, MessengerRNA, RibosomalRNA, TransferTRMU protein, humantRNA Methyltransferases

Identifiers

PMID15944150
PMCPMC2905382
OpenAlexW2034873621

What OpenQuestion holds

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Registered trials

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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.