Evidence map›Paper›PMID 10090730›Full record

ArticleGenes & development1999

Antagonism between RSF1 and SR proteins for both splice-site recognition in vitro and Drosophila development.

E Labourier, H M Bourbon, I E Gallouzi, M Fostier, E Allemand, J Tazi

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed, 57 citations in OpenAlex.

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  10. Aberrant splicing of HTT generates the pathogenic exon 1 protein in Huntington disease.Proceedings of the National Academy of Sciences of the United States of America · 2013
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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

6 authors at 3 institutions in 1 country.

E LabourierInstitut de Génétique Moléculaire, Centre National de la Recherche Scientifique (CNRS), F34293 Montpellier Cedex 5, France.
H M Bourbon
I E Gallouzi
M Fostier
E Allemand
J Tazi
Centre de Biologie du Développement · FRCentre National de la Recherche Scientifique · FRLaboratoire de Microbiologie et Génétique Moléculaires · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Specific recognition of splice sites within metazoan mRNA precursors (pre-mRNAs) is a potential stage for gene regulation by alternative splicing. Splicing factors of the SR protein family play a major role in this regulation, as they are required for early recognition of splice sites during spliceosome assembly. Here, we describe the characterization of RSF1, a splicing repressor isolated from Drosophila, that functionally antagonizes SR proteins. Like the latter, RSF1 comprises an amino-terminal RRM-type RNA-binding domain, whereas its carboxy-terminal part is enriched in glycine (G), arginine (R), and serine (S) residues (GRS domain). RSF1 induces a dose-sensitive inhibition of splicing for several reporter pre-mRNAs, an inhibition that occurs at the level of early splicing complexes formation. RSF1 interacts, through its GRS domain, with the RS domain of the SR protein SF2/ASF and prevents the latter from cooperating with the U1 small nuclear ribonucleoprotein particle (U1 snRNP) in binding pre-mRNA. Furthermore, overproduction of RSF 1 in the fly rescues several developmental defects caused by overexpression of the splicing activator SR protein B52/ SRp55. Therefore, RSF1 may correspond to the prototypical member of a novel family of general splicing repressors that selectively antagonize the effect of SR proteins on 5' splice-site recognition.

Indexed as

RNA SplicingAnimalsBase SequenceBinding, CompetitiveDNA PrimersDrosophilaProteinsRibonucleoprotein, U1 Small NuclearDNA PrimersProteinsRibonucleoprotein, U1 Small Nuclear

Identifiers

PMID10090730
PMCPMC316549
OpenAlexW2141740778

What OpenQuestion holds

Texttitle and abstract
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.