Evidence map›Paper›PMID 11564888›Full record

ArticleMolecular and cellular biology2001

Hpr1 is preferentially required for transcription of either long or G+C-rich DNA sequences in Saccharomyces cerevisiae.

S Chávez, M García-Rubio, F Prado, A Aguilera

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

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3 · Its place in the literature

Who cites it

64 citing papers in PubMed, 112 citations in OpenAlex.

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4 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

S ChávezDepartamento de Genética, Facultad de Biología, Universidad de Sevilla, 41012 Seville, Spain.
M García-Rubio
F Prado
A Aguilera
Universidad de Sevilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hpr1 forms, together with Tho2, Mft1, and Thp2, the THO complex, which controls transcription elongation and genome stability in Saccharomyces cerevisiae. Mutations in genes encoding the THO complex confer strong transcription-impairment and hyperrecombination phenotypes in the bacterial lacZ gene. In this work we demonstrate that Hpr1 is a factor required for transcription of long as well as G+C-rich DNA sequences. Using different lacZ segments fused to the GAL1 promoter, we show that the negative effect of lacZ sequences on transcription depends on their distance from the promoter. In parallel, we show that transcription of either a long LYS2 fragment or the S. cerevisiae YAT1 G+C-rich open reading frame fused to the GAL1 promoter is severely impaired in hpr1 mutants, whereas transcription of LAC4, the Kluyveromyces lactis ortholog of lacZ but with a lower G+C content, is only slightly affected. The hyperrecombination behavior of the DNA sequences studied is consistent with the transcriptional defects observed in hpr1 cells. These results indicate that both length and G+C content are important elements influencing transcription in vivo. We discuss their relevance for the understanding of the functional role of Hpr1 and, by extension, the THO complex.

Indexed as

Saccharomyces cerevisiae ProteinsTranscription, GeneticBinding SitesBlotting, NorthernDNAFungal ProteinsLac OperonModels, GeneticNuclear ProteinsNucleosomesOpen Reading FramesPlasmidsPromoter Regions, GeneticProtein BindingRecombinant Fusion ProteinsRecombination, GeneticDNAFungal ProteinsHPR1 protein, S cerevisiaeNuclear ProteinsNucleosomesRecombinant Fusion ProteinsRNA, MessengerSaccharomyces cerevisiae Proteins

Identifiers

PMID11564888
PMCPMC99881
OpenAlexW2019379779

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.