Evidence map›Paper›PMID 22474355›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Heterochromatin protein 1 homologue Swi6 acts in concert with Ers1 to regulate RNAi-directed heterochromatin assembly.

Aki Hayashi, Mayumi Ishida, Rika Kawaguchi, Takeshi Urano, Yota Murakami, Jun-ichi Nakayama

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. PhpCNature communications · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Ten principles of heterochromatin formation and function.Nature reviews. Molecular cell biology · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. RNAi and heterochromatin assembly.Cold Spring Harbor perspectives in biology · 2015
    Review
  18. Review
  19. The CINs of the centromere.Biochemical Society transactions · 2013
    Review
  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

6 authors at 4 institutions in 1 country.

Aki HayashiLaboratory for Chromatin Dynamics, RIKEN Center for Developmental Biology, Kobe, Hyogo 650-0047, Japan.
Mayumi Ishida
Rika Kawaguchi
Takeshi Urano
Yota Murakami
Jun-ichi Nakayama
RIKEN Center for Biosystems Dynamics Research · JPHokkaido University · JPKwansei Gakuin University · JPShimane University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In fission yeast, the RNAi pathway is required for centromeric heterochromatin assembly. siRNAs derived from centromeric transcripts are incorporated into the RNA-induced transcriptional silencing (RITS) complex and direct it to nascent homologous transcripts. The RNA-induced transcriptional silencing-bound nascent transcripts further recruit the RNA-directed RNA polymerase complex (RDRC) to promote dsRNA synthesis and siRNA production. Heterochromatin coated with Swi6/Heterochromain Protein 1 is then formed following recruitment of chromatin modification machinery. Swi6 is also required for the upstream production of siRNA, although the mechanism for this has remained obscure. Here, we demonstrate that Swi6 recruits RDRC to heterochromatin through Ers1, an RNAi factor intermediate. An ers1(+) mutant allele (ers1-C62) was identified in a genetic screen for mutants that alleviate centromeric silencing, and this phenotype was suppressed by overexpression of either the Hrr1 RDRC subunit or Clr4 histone H3-K9 methyltransferase. Ers1 physically interacts with Hrr1, and loss of Ers1 impairs RDRC centromeric localization. Although Ers1 failed to bind Clr4, a direct interaction with Swi6 was detected, and centromeric localization of Swi6 was enhanced by Clr4 overexpression in ers1-C62 cells. Consistent with this, deletion of swi6(+) reduced centromeric localization of Ers1 and RDRC. Moreover, tethering of Ers1 or Hrr1 to centromeric heterochromatin partially bypassed Swi6 function. These findings demonstrate an alternative mechanism for RDRC recruitment and explain the essential role of Swi6/Heterochromain Protein 1 in RNAi-directed heterochromatin assembly.

Indexed as

Blotting, WesternCell Cycle ProteinsCentromereChromatin ImmunoprecipitationChromosomal Proteins, Non-HistoneGreen Fluorescent ProteinsHeterochromatinHistone-Lysine N-MethyltransferaseMethyltransferasesMicroscopy, FluorescenceMutationProtein BindingReverse Transcriptase Polymerase Chain ReactionRNA-Dependent RNA PolymeraseRNA, FungalRNA-Induced Silencing ComplexCell Cycle ProteinsChromosomal Proteins, Non-Histoneclr4 protein, S pombeErs1 protein, S pombeGreen Fluorescent ProteinsHeterochromatinHistone-Lysine N-MethyltransferaseMethyltransferasesRNA-Dependent RNA PolymeraseRNA, FungalRNA-Induced Silencing ComplexRNA, Small InterferingSchizosaccharomyces pombe ProteinsSwi6 protein, S pombe

Identifiers

PMID22474355
PMCPMC3341003
OpenAlexW2158581721

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.