Evidence map›Paper›PMID 7739552›Full record

ArticleMolecular and cellular biology1995

Synthetic lethality of sep1 (xrn1) ski2 and sep1 (xrn1) ski3 mutants of Saccharomyces cerevisiae is independent of killer virus and suggests a general role for these genes in translation control.

A W Johnson, R D Kolodner

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
14.5field-weighted citation impact, top 1% 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

56 citing papers in PubMed, 99 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The KillerMicroorganisms · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Diverse yeast antiviral systems prevent lethal pathogenesis caused by the L-A mycovirus.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  9. Article
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  14. Article
  15. Article
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  17. Meiotic viral attenuation through an ancestral apoptotic pathway.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  18. Article
  19. 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

2 authors at 2 institutions in 1 country.

A W JohnsonDivision of Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
R D Kolodner
Dana-Farber Cancer Institute · USHarvard University · US

Funding

VectorP30CA006516 · NCI · DANA-FARBER CANCER INSTITUTE · PI A. Heather Eliassen · 1985 to 2026
$330.6M
STRUCTURE AND FUNCTION OF YEAST STRAND EXCHANGE PROTEINF32GM013594 · NIGMS · DANA-FARBER CANCER INSTITUTE · PI JOHNSON, ARLEN W · 1990 to 1992
–
MOLECULAR MECHANISMS OF GENETIC RECOMBINATION IN YEASTR01GM029383 · NIGMS · DANA-FARBER CANCER INSTITUTE · PI KOLODNER, RICHARD D · 1985 to 1994
–
NCI NIH HHS CA06516NIGMS NIH HHS GM13594NIGMS NIH HHS GM29383
6 · The paper itself

Abstract

Strand exchange protein 1 (Sep1) (also referred to as exoribonuclease I [Xrn1]) from Saccharomyces cerevisiae has been implicated in DNA recombination, RNA turnover, karyogamy, and G4 DNA pairing among other disparate cellular processes. Using a genetic approach to study the role of SEP1/XRN1 in mitotic yeast cells, we identified mutations in the genes superkiller 2 (SKI2) and superkiller 3 (SKI3) as synthetically lethal with an sep1 null mutation. The SKI genes are thought to comprise an intracellular antiviral system controlling the expression of killer toxin from double-stranded RNA virus found in many yeast strains. However, the lethality of sep1 ski2 and sep1 ski3 mutants was independent of the L-A and M viruses, suggesting that the SKI genes act in a general cellular process in addition to virus control. We propose that Sep1/Xrn1 and Ski2 both act to block translation on transcripts targeted for degradation. Using a temperature-sensitive allele of SEP1/XRN1, we show that double mutants display a synthetic cell cycle arrest in late G1 at Start.

Indexed as

ExoribonucleasesGenes, FungalMutationSaccharomyces cerevisiae ProteinsBase SequenceDeoxyribonucleasesDNA, FungalDNA PrimersFungal ProteinsG1 PhaseGenes, LethalMolecular Sequence DataPhenotypeProtein BiosynthesisSaccharomyces cerevisiaeDeoxyribonucleasesDNA, FungalDNA PrimersExoribonucleasesFungal ProteinsSaccharomyces cerevisiae ProteinsSKI2 protein, S cerevisiaeXRN1 protein, S cerevisiae

Identifiers

PMID7739552
PMCPMC230502
OpenAlexW2151879743

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.