Evidence map›Paper›PMID 26279681›Full record

ArticleEpigenetics & chromatin2015

Role of Ccr4-Not complex in heterochromatin formation at meiotic genes and subtelomeres in fission yeast.

Cristina Cotobal, María Rodríguez-López, Caia Duncan, Ayesha Hasan, Akira Yamashita, Masayuki Yamamoto, Jürg Bähler, Juan Mata

Open access · goldAbstract read
In one paragraph

Article in Epigenetics & chromatin, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 47 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

8 authors at 3 institutions in 2 countries.

Cristina CotobalDepartment of Biochemistry, University of Cambridge, Cambridge, UK.
María Rodríguez-LópezDepartment of Genetics, Evolution and Environment, UCL Cancer Institute, University College London, London, UK.
Caia DuncanDepartment of Biochemistry, University of Cambridge, Cambridge, UK.
Ayesha HasanDepartment of Biochemistry, University of Cambridge, Cambridge, UK.
Akira YamashitaLaboratory of Cell Responses, National Institute for Basic Biology, Okazaki, Japan.
Masayuki YamamotoLaboratory of Cell Responses, National Institute for Basic Biology, Okazaki, Japan.
Jürg BählerDepartment of Genetics, Evolution and Environment, UCL Cancer Institute, University College London, London, UK.
Juan MataDepartment of Biochemistry, University of Cambridge, Cambridge, UK.
University of Cambridge · GBNational Institute for Basic Biology · JPUniversity College London · GB

Funding

Biotechnology and Biological Sciences Research Council BB/J007153/1Wellcome Trust 095598
6 · The paper itself

Abstract

backgroundHeterochromatin is essential for chromosome segregation, gene silencing and genome integrity. The fission yeast Schizosaccharomyces pombe contains heterochromatin at centromeres, subtelomeres, and mating type genes, as well as at small islands of meiotic genes dispersed across the genome. This heterochromatin is generated by partially redundant mechanisms, including the production of small interfering RNAs (siRNAs) that are incorporated into the RITS protein complex (RNAi-Induced Transcriptional Silencing). The assembly of heterochromatin islands requires the function of the RNA-binding protein Mmi1, which recruits RITS to its mRNA targets and to heterochromatin islands. In addition, Mmi1 directs its targets to an exosome-dependent RNA elimination pathway.

resultsCcr4-Not is a conserved multiprotein complex that regulates gene expression at multiple levels, including RNA degradation and translation. We show here that Ccr4-Not is recruited by Mmi1 to its RNA targets. Surprisingly, Ccr4 and Caf1 (the mRNA deadenylase catalytic subunits of the Ccr4-Not complex) are not necessary for the degradation or translation of Mmi1 RNA targets, but are essential for heterochromatin integrity at Mmi1-dependent islands and, independently of Mmi1, at subtelomeric regions. Both roles require the deadenylase activity of Ccr4 and the Mot2/Not4 protein, a ubiquitin ligase that is also part of the complex. Genetic evidence shows that Ccr4-mediated silencing is essential for normal cell growth, indicating that this novel regulation is physiologically relevant. Moreover, Ccr4 interacts with components of the RITS complex in a Mmi1-independent manner.

conclusionsTaken together, our results demonstrate that the Ccr4-Not complex is required for heterochromatin integrity in both Mmi1-dependent and Mmi1-independent pathways.

Indexed as

Ccr4-Not complexChIP-seqGenome-wide approachesHeterochromatinRIP-chipS. pombe

Identifiers

PMID26279681
PMCPMC4536793
OpenAlexW1790852709

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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.