Evidence map›Paper›PMID 20807763›Full record

ArticleThe Journal of biological chemistry2010

The carboxyl-terminal end of Cox1 is required for feedback assembly regulation of Cox1 synthesis in Saccharomyces cerevisiae mitochondria.

Miguel Shingú-Vázquez, Yolanda Camacho-Villasana, Luisa Sandoval-Romero, Christine A Butler, Thomas D Fox, Xochitl Pérez-Martínez

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. The cytochromeLife science alliance · 2023
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The Cox1 C-terminal domain is a central regulator of cytochromeThe Journal of biological chemistry · 2017
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

6 authors at 3 institutions in 2 countries.

Miguel Shingú-VázquezDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México DF 04510, México.
Yolanda Camacho-Villasana
Luisa Sandoval-Romero
Christine A Butler
Thomas D Fox
Xochitl Pérez-Martínez
Universidad Nacional Autónoma de México · MXCornell University · USInstituto Nacional de Rehabilitación · MX

Funding

TRANSLATIONAL CONTROL OF YEAST MITOCHONDRIAL GENESR01GM029362 · NIGMS · CORNELL UNIVERSITY ITHACA · PI FOX, THOMAS DAVID · 1985 to 2013
$6.1M
NIGMS NIH HHS GM029362NIGMS NIH HHS R01 GM029362
6 · The paper itself

Abstract

Synthesis of the largest cytochrome c oxidase (CcO) subunit, Cox1, on yeast mitochondrial ribosomes is coupled to assembly of CcO. The translational activator Mss51 is sequestered in early assembly intermediate complexes by an interaction with Cox14 that depends on the presence of newly synthesized Cox1. If CcO assembly is prevented, the level of Mss51 available for translational activation is reduced. We deleted the C-terminal 11 or 15 residues of Cox1 by site-directed mutagenesis of mtDNA. Although these deletions did not prevent respiratory growth of yeast, they eliminated the assembly-feedback control of Cox1 synthesis. Furthermore, these deletions reduced the strength of the Mss51-Cox14 interaction as detected by co-immunoprecipitation, confirming the importance of the Cox1 C-terminal residues for Mss51 sequestration. We surveyed a panel of mutations that block CcO assembly for the strength of their effect on Cox1 synthesis, both by pulse labeling and expression of the ARG8(m) reporter fused to COX1. Deletion of the nuclear gene encoding Cox6, one of the first subunits to be added to assembling CcO, caused the most severe reduction in Cox1 synthesis. Deletion of the C-terminal 15 amino acids of Cox1 increased Cox1 synthesis in the presence of each of these mutations, except pet54. Our data suggest a novel activity of Pet54 required for normal synthesis of Cox1 that is independent of the Cox1 C-terminal end.

Indexed as

Amino Acid SequenceElectron Transport Complex IVMembrane ProteinsMitochondriaMitochondrial ProteinsRNA-Binding ProteinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSequence DeletionTranscription FactorsTranscription, GeneticCOX14 protein, S cerevisiaeCox1 protein, S cerevisiaeElectron Transport Complex IVMembrane ProteinsMitochondrial ProteinsMss51 protein, S cerevisiaePet54 protein, S cerevisiaeRNA-Binding ProteinsSaccharomyces cerevisiae ProteinsTranscription Factors

Identifiers

PMID20807763
PMCPMC2966052
OpenAlexW2062468477

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.