Evidence map›Paper›PMID 35977387›Full record

ArticleGenetics2022

Suppressor mutations that make the essential transcription factor Spn1/Iws1 dispensable in Saccharomyces cerevisiae.

Francheska López-Rivera, James Chuang, Dan Spatt, Rajaraman Gopalakrishnan, Fred Winston

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Francheska López-RiveraDepartment of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0002-5160-6120
James ChuangDepartment of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0002-9802-1808
Dan SpattDepartment of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Rajaraman GopalakrishnanDepartment of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Fred WinstonDepartment of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0002-4759-5537
Harvard University · US

Funding

Genetics and Genomics PhD Training GrantT32GM096911 · NIGMS · HARVARD MEDICAL SCHOOL · PI KENNEDY, SCOTT G · 2011 to 2020
$2.5M
Analysis of the Essential Transcription Factors Spt5 and Spn1/Iws1R01GM120038 · NIGMS · HARVARD MEDICAL SCHOOL · PI WINSTON, FRED M. · 2017 to 2020
$2.0M
NIGMS NIH HHS R01 GM120038NIGMS NIH HHS T32 GM096911NIH HHS R01GM120038
6 · The paper itself

Abstract

Spn1/Iws1 is an essential eukaryotic transcription elongation factor that is conserved from yeast to humans as an integral member of the RNA polymerase II elongation complex. Several studies have shown that Spn1 functions as a histone chaperone to control transcription, RNA splicing, genome stability, and histone modifications. However, the precise role of Spn1 is not understood, and there is little understanding of why it is essential for viability. To address these issues, we have isolated 8 suppressor mutations that bypass the essential requirement for Spn1 in Saccharomyces cerevisiae. Unexpectedly, the suppressors identify several functionally distinct complexes and activities, including the histone chaperone FACT, the histone methyltransferase Set2, the Rpd3S histone deacetylase complex, the histone acetyltransferase Rtt109, the nucleosome remodeler Chd1, and a member of the SAGA coactivator complex, Sgf73. The identification of these distinct groups suggests that there are multiple ways in which Spn1 bypass can occur, including changes in histone acetylation and alterations in other histone chaperones. Thus, Spn1 may function to overcome repressive chromatin by multiple mechanisms during transcription. Our results suggest that bypassing a subset of these functions allows viability in the absence of Spn1.

Indexed as

Saccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranscriptional Elongation FactorsChromatinDNA-Binding ProteinsHistone AcetyltransferasesHistone ChaperonesHistone DeacetylasesHistone MethyltransferasesHistonesNucleosomesPeptide Elongation FactorsRNA-Binding ProteinsRNA Polymerase IISuppression, GeneticTranscription FactorsCHD1 protein, S cerevisiaeChromatinDNA-Binding ProteinsHistone AcetyltransferasesHistone ChaperonesHistone DeacetylasesHistone MethyltransferasesHistonesIWS1 protein, S cerevisiaeNucleosomesPeptide Elongation FactorsRNA-Binding ProteinsRNA Polymerase IISaccharomyces cerevisiae ProteinsSPN1 protein, S cerevisiaeTranscriptional Elongation FactorsTranscription Factorschromatinhistone chaperoneIws1Spn1transcription

Identifiers

PMID35977387
PMCPMC9526074
OpenAlexW4292261311

What OpenQuestion holds

Textmetadata
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.