Evidence map›Paper›PMID 28062854›Full record

ArticleNucleic acids research2017

SF3b1 mutations associated with myelodysplastic syndromes alter the fidelity of branchsite selection in yeast.

Tucker J Carrocci, Douglas M Zoerner, Joshua C Paulson, Aaron A Hoskins

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 85 citations in OpenAlex.

  1. Control of 3' splice site selection inRNA (New York, N.Y.) · 2025
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Control of 3' splice site selection by the yeast splicing factor Fyv6.bioRxiv : the preprint server for biology · 2024
    Article
  7. Article
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  11. Functional Analysis of the Zinc Finger Modules of thebioRxiv : the preprint server for biology · 2024
    Article
  12. Article
  13. Life science alliance · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Impacts and mechanisms of alternative mRNA splicing in cancer metabolism, immune response, and therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Review
  19. Article
  20. Article
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.

Tucker J CarrocciDepartment of Biochemistry, U. Wisconsin-Madison, Madison, WI 53706, USA.
Douglas M ZoernerDepartment of Biochemistry, U. Wisconsin-Madison, Madison, WI 53706, USA.
Joshua C PaulsonDepartment of Biochemistry, U. Wisconsin-Madison, Madison, WI 53706, USA.
Aaron A HoskinsDepartment of Biochemistry, U. Wisconsin-Madison, Madison, WI 53706, USA.
University of Wisconsin–Madison · US

Funding

BIOTECHNOLOGY TRAINING PROGRAMT32GM008349 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI FOX, BRIAN G · 1989 to 2019
$22.5M
Mechanisms of Spliceosome Assembly and Splice Site RecognitionR01GM112735 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI HOSKINS, AARON ANDREW · 2015 to 2019
$1.6M
Mechanisms of Spliceosome Assembly and Splice Site SelectionR00GM086471 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI HOSKINS, AARON ANDREW · 2011 to 2013
$733k
NIGMS NIH HHS R00 GM086471NIGMS NIH HHS R01 GM112735NIGMS NIH HHS T32 GM008349
6 · The paper itself

Abstract

RNA and protein components of the spliceosome work together to identify the 5΄ splice site, the 3΄ splice site, and the branchsite (BS) of nascent pre-mRNA. SF3b1 plays a key role in recruiting the U2 snRNP to the BS. Mutations in human SF3b1 have been linked to many diseases such as myelodysplasia (MDS) and cancer. We have used SF3b1 mutations associated with MDS to interrogate the role of the yeast ortholog, Hsh155, in BS selection and splicing. These alleles change how the spliceosome recognizes the BS and alter splicing when nonconsensus nucleotides are present at the -2, -1 and +1 positions relative to the branchpoint adenosine. This indicates that changes in BS usage observed in humans with SF3b1 mutations may result from perturbation of a conserved mechanism of BS recognition. Notably, different HSH155 alleles elicit disparate effects on splicing: some increase the fidelity of BS selection while others decrease fidelity. Our data support a model wherein conformational changes in SF3b1 promote U2 association with the BS independently of the action of the DEAD-box ATPase Prp5. We propose that SF3b1 functions to stabilize weak U2/BS duplexes to drive spliceosome assembly and splicing.

Indexed as

Adenosine TriphosphatasesDEAD-box RNA HelicasesHumansMutationMyelodysplastic SyndromesPhosphoproteinsRibonucleoprotein, U2 Small NuclearRNA SplicingRNA Splicing FactorsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSpliceosomesAdenosine TriphosphatasesDDX46 protein, humanDEAD-box RNA HelicasesHSH155 protein, S cerevisiaePhosphoproteinsPRP5 protein, S cerevisiaeRibonucleoprotein, U2 Small NuclearRNA Splicing FactorsSaccharomyces cerevisiae ProteinsSF3B1 protein, human

Identifiers

PMID28062854
PMCPMC5416834
OpenAlexW2570514707

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.