Evidence map›Paper›PMID 20838586›Full record

ArticlePLoS genetics2010

Perturbation analysis of heterochromatin-mediated gene silencing and somatic inheritance.

Jonathan I Schneiderman, Sara Goldstein, Kami Ahmad

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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  8. Samd7 is a cell type-specific PRC1 component essential for establishing retinal rod photoreceptor identity.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Article
  10. Birth of a new gene on the Y chromosome of Drosophila melanogaster.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
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  12. Review
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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

3 authors at 1 institution in 1 country.

Jonathan I SchneidermanDepartment of BCMP, Harvard Medical School, Boston, Massachusetts, United States of America.
Sara Goldstein
Kami Ahmad
Harvard University · US

Funding

Histone Variants and Transcription-linked DepositionR01GM068696 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI AHMAD, KAMRAN · 2004 to 2008
$1.6M
NIGMS NIH HHS GM068696NIGMS NIH HHS R01 GM068696
6 · The paper itself

Abstract

Repetitive sequences in eukaryotic genomes induce chromatin-mediated gene-silencing of juxtaposed genes. Many components that promote or antagonize silencing have been identified, but how heterochromatin causes variegated and heritable changes in gene expression remains mysterious. We have used inducible mis-expression in the Drosophila eye to recover new factors that alter silencing caused by the bw(D) allele, an insertion of repetitive satellite DNA that silences a bw(+) allele on the homologous chromosome. Inducible modifiers allow perturbation of silencing at different times in development, and distinguish factors that affect establishment or maintenance of silencing. We find that diverse chromatin and RNA processing factors can de-repress silencing. Most factors are effective even in differentiated cells, implying that silent chromatin remains plastic. However, over-expression of the bantam microRNA or the crooked-legs (crol) zinc-finger protein only de-repress silencing when expressed in cycling cells. Over-expression of crol accelerates the cell cycle, and this is required for de-repression of silencing. Strikingly, continual over-expression of crol converts the speckled variegation pattern of bw(D) into sectored variegation, where de-repression is stably inherited through mitotic divisions. Over-expression of crol establishes an open chromatin state, but the factor is not needed to maintain this state. Our analysis reveals that active chromatin states can be efficiently inherited through cell divisions, with implications for the stable maintenance of gene expression patterns through development.

Indexed as

Gene SilencingAnimalsCell CycleDrosophila melanogasterDrosophila ProteinsEnhancer Elements, GeneticEyeHeterochromatinInheritance PatternsMicroRNAsNuclear ProteinsRepressor ProteinsRNA InterferenceTranscription Factorsbantam microRNA, Drosophilacrol protein, DrosophilaDrosophila ProteinsHeterochromatinMicroRNAsNuclear ProteinsRepressor ProteinsTranscription Factors

Identifiers

PMID20838586
PMCPMC2936522
OpenAlexW2007030194

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.