Evidence map›Paper›PMID 21149581›Full record

ArticleMolecular and cellular biology2011

Genomic mRNA profiling reveals compensatory mechanisms for the requirement of the essential splicing factor U2AF.

Vinod Sridharan, Joseph Heimiller, Ravinder Singh

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

17 citing papers in PubMed.

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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

3 authors.

Vinod SridharanDepartment of Molecular, Cellular and Developmental Biology, University of Colorado at Boulder, Boulder, CO 80309, USA.
Joseph Heimiller
Ravinder Singh

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The large subunit of the U2 auxiliary factor (U2AF) recognizes the polypyrimidine tract (Py-tract) located adjacent to the 3' splice site to facilitate U2 snRNP recruitment. While U2AF is considered essential for pre-mRNA splicing, its requirement for splicing on a genome-wide level has not been analyzed. Using Solexa sequencing, we performed mRNA profiling for splicing in the Schizosaccharomyces pombe U2AF(59) (prp2.1) temperature-sensitive mutant. Surprisingly, our analysis revealed that introns show a range of splicing defects in the mutant strain. While U2AF(59) inactivation (nonpermissive) conditions inhibit splicing of some introns, others are spliced apparently normally. Bioinformatics analysis indicated that U2AF(59)-insensitive introns have stronger 5' splice sites and higher A/U content. Most importantly, features that contribute to U2AF(59) insensitivity of an intron unexpectedly reside in its 5'-most 30 nucleotides. These include the 5' splice site, a guanosine at position 7, and the 5' splice site-to-branch point sequence context. A differential requirement (similar to U2AF(59)) for introns may also apply to other general splicing factors (e.g., prp10). Our combined results indicate that U2AF insensitivity is a common phenomenon and that varied intron features support the existence of unrecognized aspects of spliceosome assembly.

Indexed as

Base SequenceGene Expression ProfilingGenome, FungalIntronsModels, BiologicalMolecular Sequence DataMutationNuclear ProteinsRibonucleoproteinsRNA, FungalRNA, MessengerRNA Splice SitesRNA SplicingSchizosaccharomycesSchizosaccharomyces pombe ProteinsSpliceosomesNuclear ProteinsRibonucleoproteinsRNA, FungalRNA, MessengerRNA Splice SitesSchizosaccharomyces pombe ProteinsSplicing Factor U2AF

Identifiers

PMID21149581
PMCPMC3028654

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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.