Evidence map›Paper›PMID 26848854›Full record

ArticlePloS one2016

Recruitment of Saccharomyces cerevisiae Cmr1/Ydl156w to Coding Regions Promotes Transcription Genome Wide.

Jeffery W Jones, Priyanka Singh, Chhabi K Govind

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. An integrated structural model of the DNA damage-responsive H3K4me3 binding WDR76:SPIN1 complex with the nucleosome.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. Article
  3. The role of WDR76 protein in human diseases.Bosnian journal of basic medical sciences · 2021
    Review
  4. Article
  5. Article
  6. 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

3 authors at 1 institution in 1 country.

Jeffery W JonesDepartment of Biological Sciences, Oakland University, Rochester, MI-48309, United States of America.
Priyanka SinghDepartment of Biological Sciences, Oakland University, Rochester, MI-48309, United States of America.
Chhabi K GovindDepartment of Biological Sciences, Oakland University, Rochester, MI-48309, United States of America.
Oakland University · US

Funding

Mechanisms of RSC recruitment and its role in transcriptionR01GM095514 · NIGMS · OAKLAND UNIVERSITY · PI GOVIND, CHHABI K · 2011 to 2015
$1.5M
NIGMS NIH HHS GM095514NIGMS NIH HHS R01 GM095514
6 · The paper itself

Abstract

Cmr1 (changed mutation rate 1) is a largely uncharacterized nuclear protein that has recently emerged in several global genetic interaction and protein localization studies. It clusters with proteins involved in DNA damage and replication stress response, suggesting a role in maintaining genome integrity. Under conditions of proteasome inhibition or replication stress, this protein localizes to distinct sub-nuclear foci termed as intranuclear quality control (INQ) compartments, which sequester proteins for their subsequent degradation. Interestingly, it also interacts with histones, chromatin remodelers and modifiers, as well as with proteins involved in transcription including subunits of RNA Pol I and Pol III, but not with those of Pol II. It is not known whether Cmr1 plays a role in regulating transcription of Pol II target genes. Here, we show that Cmr1 is recruited to the coding regions of transcribed genes of S. cerevisiae. Cmr1 occupancy correlates with the Pol II occupancy genome-wide, indicating that it is recruited to coding sequences in a transcription-dependent manner. Cmr1-enriched genes include Gcn4 targets and ribosomal protein genes. Furthermore, our results show that Cmr1 recruitment to coding sequences is stimulated by Pol II CTD kinase, Kin28, and the histone deacetylases, Rpd3 and Hos2. Finally, our genome-wide analyses implicate Cmr1 in regulating Pol II occupancy at transcribed coding sequences. However, it is dispensable for maintaining co-transcriptional histone occupancy and histone modification (acetylation and methylation). Collectively, our results show that Cmr1 facilitates transcription by directly engaging with transcribed coding regions.

Indexed as

Transcription, GeneticCyclin-Dependent KinasesDNA-Binding ProteinsGenome, FungalHistone CodeHistone DeacetylasesHistonesOpen Reading FramesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCmr1 protein, S cerevisiaeCyclin-Dependent KinasesDNA-Binding ProteinsHistone DeacetylasesHistonesHOS2 protein, S cerevisiaeKin28 protein kinase, S cerevisiaeRPD3 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID26848854
PMCPMC4744024
OpenAlexW2279286887

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.