Evidence map›Paper›PMID 36617881›Full record

ArticleGenes & development

Tandemly repeated genes promote RNAi-mediated heterochromatin formation via an antisilencing factor, Epe1, in fission yeast.

Takahiro Asanuma, Soichi Inagaki, Tetsuji Kakutani, Hiroyuki Aburatani, Yota Murakami

Open access · diamondAbstract read
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Article in Genes & development. 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
–field-weighted citation impact
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, 13 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 3 institutions in 1 country.

Takahiro AsanumaDepartment of Chemistry, Faculty of Science, Hokkaido University, Sapporo 060-0810, Japan.
Soichi InagakiDepartment of Biological Sciences, Faculty of Science, University of Tokyo, Tokyo 113-0033, Japan.ORCID 0000-0003-4090-826X
Tetsuji KakutaniDepartment of Biological Sciences, Faculty of Science, University of Tokyo, Tokyo 113-0033, Japan.ORCID 0000-0002-6137-4474
Hiroyuki AburataniGenome Science Division, Research Center for Advanced Science and Technology, University of Tokyo, Tokyo 153-8904, Japan.
Yota MurakamiDepartment of Chemistry, Faculty of Science, Hokkaido University, Sapporo 060-0810, Japan.ORCID 0000-0002-2023-1303
Hokkaido University · JPTokyo University of Science · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In most eukaryotes, constitutive heterochromatin, defined by histone H3 lysine 9 methylation (H3K9me), is enriched on repetitive DNA, such as pericentromeric repeats and transposons. Furthermore, repetitive transgenes also induce heterochromatin formation in diverse model organisms. However, the mechanisms that promote heterochromatin formation at repetitive DNA elements are still not clear. Here, using fission yeast, we show that tandemly repeated mRNA genes promote RNA interference (RNAi)-mediated heterochromatin formation in cooperation with an antisilencing factor, Epe1. Although the presence of tandemly repeated genes itself does not cause heterochromatin formation, once complementary small RNAs are artificially supplied in

Indexed as

SchizosaccharomycesSchizosaccharomyces pombe ProteinsHeterochromatinHistonesNuclear ProteinsRNA Interferenceepe1 protein, S pombeHeterochromatinHistonesNuclear ProteinsSchizosaccharomyces pombe ProteinsEpe1fission yeastheterochromatinrepetitive DNARIGSRNAiRNA interference

Identifiers

PMID36617881
PMCPMC9851402
OpenAlexW4313447968

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

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.