Evidence map›Paper›PMID 31465447›Full record

ArticlePLoS genetics2019

SSD1 suppresses phenotypes induced by the lack of Elongator-dependent tRNA modifications.

Fu Xu, Anders S Byström, Marcus J O Johansson

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 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
0.7field-weighted citation impact, top 31% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  8. tRNA epitranscriptome determines pathogenicity of the opportunistic pathogenProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. Article
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  11. Role ofInternational journal of molecular sciences · 2021
    Article
  12. Review
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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

3 authors at 1 institution in 1 country.

Fu XuDepartment of Molecular Biology, Umeå University, Umeå, Sweden.ORCID 0000-0003-3299-6415
Anders S ByströmDepartment of Molecular Biology, Umeå University, Umeå, Sweden.ORCID 0000-0003-1281-3888
Marcus J O JohanssonDepartment of Molecular Biology, Umeå University, Umeå, Sweden.ORCID 0000-0001-7117-7426
Umeå University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Elongator complex promotes formation of 5-methoxycarbonylmethyl (mcm5) and 5-carbamoylmethyl (ncm5) side-chains on uridines at the wobble position of cytosolic eukaryotic tRNAs. In all eukaryotic organisms tested to date, the inactivation of Elongator not only leads to the lack of mcm5/ncm5 groups in tRNAs, but also a wide variety of additional phenotypes. Although the phenotypes are most likely caused by a translational defect induced by reduced functionality of the hypomodified tRNAs, the mechanism(s) underlying individual phenotypes are poorly understood. In this study, we show that the genetic background modulates the phenotypes induced by the lack of mcm5/ncm5 groups in Saccharomyces cerevisiae. We show that the stress-induced growth defects of Elongator mutants are stronger in the W303 than in the closely related S288C genetic background and that the phenotypic differences are caused by the known polymorphism at the locus for the mRNA binding protein Ssd1. Moreover, the mutant ssd1 allele found in W303 cells is required for the reported histone H3 acetylation and telomeric gene silencing defects of Elongator mutants. The difference at the SSD1 locus also partially explains why the simultaneous lack of mcm5 and 2-thio groups at wobble uridines is lethal in the W303 but not in the S288C background. Collectively, our results demonstrate that the SSD1 locus modulates phenotypes induced by the lack of Elongator-dependent tRNA modifications.

Indexed as

Gene ExpressionGenotypeHistone AcetyltransferasesPeptide Elongation FactorsPhenotypeRNA-Binding ProteinsRNA Processing, Post-TranscriptionalRNA, TransferSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsUridine5-carbamoylmethyluridine5-methoxycarbonylmethyluridineHistone AcetyltransferasesIKI3 protein, S cerevisiaePeptide Elongation FactorsRNA-Binding ProteinsRNA, TransferSaccharomyces cerevisiae ProteinsSsd1 protein, S cerevisiaeUridine

Identifiers

PMID31465447
PMCPMC6738719
OpenAlexW2970945479

What OpenQuestion holds

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LicenceCC BY
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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.