Evidence map›Paper›PMID 17594096›Full record

ArticleCurrent genetics2007

Sfl1p acts as an activator of the HSP30 gene in Saccharomyces cerevisiae.

Virginie Ansanay Galeote, Hervé Alexandre, Benoit Bach, Pierre Delobel, Sylvie Dequin, Bruno Blondin

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Article in Current genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

6 authors.

Virginie Ansanay GaleoteUMR1083 Sciences Pour l'Oenologie, INRA, 34060 Montpellier, France. virginie.ansanay@supagro.inra.fr
Hervé Alexandre
Benoit Bach
Pierre Delobel
Sylvie Dequin
Bruno Blondin

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the yeast, environmental challenges are known to induce both specific and general stress response. The HSP30 gene is strongly induced when cells are exposed to various stresses but this activation is largely independent of the major stress-related transcription factor Hsf1p and partly independent from Msn2p/Msn4p. In order to identify new potential regulators of HSP30 we isolated insertion mutants affected in HSP30 expression. We identified SFL1 gene encoding a protein previously shown to repress several genes. We show that Sfl1 is involved in the transcriptional activation of HSP30. Mutation of sfl1 reduces HSP30-lacZ expression under both basal and stress-induced conditions. We also show, using site-directed mutagenesis, that HSL motifs (Heat-Shock-Like putative DNA binding sequence) located in HSP30 promoter are required for HSP30 activation. Finally, a genome-wide analysis of the effects of SFL1 deletion on gene expression revealed that Sfl1p controls the expression of a small number of genes, with some being activated by the protein and others repressed. As a whole our data show that Sfl1p is a key component of the transcriptional control of the stress responsive gene HSP30. Moreover, we show that Sfl1, which was previously described as being a transcriptional repressor, can also act as an activator.

Indexed as

Genes, FungalBase SequenceDNA, FungalDNA PrimersEthanolGene DeletionGene Expression Regulation, FungalGenome, FungalHSP30 Heat-Shock ProteinsLac OperonMolecular Sequence DataMutagenesis, InsertionalMutagenesis, Site-DirectedMutationOligonucleotide Array Sequence AnalysisPhenotypeDNA, FungalDNA PrimersEthanolHSP30 Heat-Shock ProteinsHSP30 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSFL1 protein, S cerevisiaeTranscription Factors

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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.