Evidence map›Paper›PMID 11139493›Full record

ArticleGenetics2001

A new hyperrecombination mutation identifies a novel yeast gene, THP1, connecting transcription elongation with mitotic recombination.

M Gallardo, A Aguilera

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.7field-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

32 citing papers in PubMed, 64 citations in OpenAlex.

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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 1 institution in 1 country.

M GallardoDepartamento de Genética, Universidad de Sevilla, 41012 Seville, Spain.
A Aguilera
Universidad de Sevilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Given the importance of the incidence of recombination in genomic instability, it is of great interest to know the elements or processes controlling recombination in mitosis. One such process is transcription, which has been shown to induce recombination in bacteria, yeast, and mammals. To further investigate the genetic control of the incidence of recombination and genetic instability and, in particular, its connection with transcription, we have undertaken a search for hyperrecombination mutants among a large number of strains deleted in genes of unknown function. We have identified a new gene, THP1 (YOL072w), whose deletion mutation strongly stimulates recombination between repeats. In addition, thp1 Delta impairs transcription, a defect that is particularly strong at the level of elongation through particular DNA sequences such as lacZ. The hyperrecombination phenotype of thp1 Delta cells is fully dependent on transcription elongation of the repeat construct. When transcription is impeded either by shutting off the promoter or by using a premature transcription terminator, hyperrecombination between repeats is abolished, providing new evidence that transcription-elongation impairment may be a source of recombinogenic substrates in mitosis. We show that Thp1p and two other proteins previously shown to control transcription-associated recombination, Hpr1p and Tho2p, act in the same "pathway" connecting transcription elongation with the incidence of mitotic recombination.

Indexed as

Genes, FungalMutationRecombination, GeneticSaccharomyces cerevisiae ProteinsAnimalsBase SequenceDNA, FungalFungal ProteinsGene DeletionHoloenzymesMitosisNuclear ProteinsRecombinant Fusion ProteinsRNA Polymerase IISaccharomyces cerevisiaeTranscription FactorsDNA, FungalFungal ProteinsHoloenzymesHPR1 protein, S cerevisiaeNuclear ProteinsRecombinant Fusion ProteinsRNA Polymerase IISaccharomyces cerevisiae ProteinsTHO2 protein, S cerevisiaeTranscription Factors

Identifiers

PMID11139493
PMCPMC1461480
OpenAlexW1943761658

What OpenQuestion holds

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Read underepoch 390

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.