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Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing

Overview of attention for article published in Epigenetics & Chromatin, May 2016
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  • In the top 25% of all research outputs scored by Altmetric
  • Good Attention Score compared to outputs of the same age (75th percentile)

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Citations

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51 Dimensions

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70 Mendeley
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1 CiteULike
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Title
Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing
Published in
Epigenetics & Chromatin, May 2016
DOI 10.1186/s13072-016-0064-6
Pubmed ID
Authors

Andrew Keniry, Linden J. Gearing, Natasha Jansz, Joy Liu, Aliaksei Z. Holik, Peter F. Hickey, Sarah A. Kinkel, Darcy L. Moore, Kelsey Breslin, Kelan Chen, Ruijie Liu, Catherine Phillips, Miha Pakusch, Christine Biben, Julie M. Sheridan, Benjamin T. Kile, Catherine Carmichael, Matthew E. Ritchie, Douglas J. Hilton, Marnie E. Blewitt

Abstract

The presence of histone 3 lysine 9 (H3K9) methylation on the mouse inactive X chromosome has been controversial over the last 15 years, and the functional role of H3K9 methylation in X chromosome inactivation in any species has remained largely unexplored. Here we report the first genomic analysis of H3K9 di- and tri-methylation on the inactive X: we find they are enriched at the intergenic, gene poor regions of the inactive X, interspersed between H3K27 tri-methylation domains found in the gene dense regions. Although H3K9 methylation is predominantly non-genic, we find that depletion of H3K9 methylation via depletion of H3K9 methyltransferase Set domain bifurcated 1 (Setdb1) during the establishment of X inactivation, results in failure of silencing for around 150 genes on the inactive X. By contrast, we find a very minor role for Setdb1-mediated H3K9 methylation once X inactivation is fully established. In addition to failed gene silencing, we observed a specific failure to silence X-linked long-terminal repeat class repetitive elements. Here we have shown that H3K9 methylation clearly marks the murine inactive X chromosome. The role of this mark is most apparent during the establishment phase of gene silencing, with a more muted effect on maintenance of the silent state. Based on our data, we hypothesise that Setdb1-mediated H3K9 methylation plays a role in epigenetic silencing of the inactive X via silencing of the repeats, which itself facilitates gene silencing through alterations to the conformation of the whole inactive X chromosome.

Twitter Demographics

The data shown below were collected from the profiles of 9 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 70 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Japan 1 1%
Unknown 69 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 18 26%
Researcher 16 23%
Student > Postgraduate 5 7%
Student > Bachelor 5 7%
Student > Master 4 6%
Other 13 19%
Unknown 9 13%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 36 51%
Agricultural and Biological Sciences 18 26%
Immunology and Microbiology 2 3%
Medicine and Dentistry 2 3%
Psychology 1 1%
Other 2 3%
Unknown 9 13%

Attention Score in Context

This research output has an Altmetric Attention Score of 6. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 05 January 2017.
All research outputs
#4,248,051
of 17,826,855 outputs
Outputs from Epigenetics & Chromatin
#177
of 497 outputs
Outputs of similar age
#67,596
of 271,995 outputs
Outputs of similar age from Epigenetics & Chromatin
#1
of 1 outputs
Altmetric has tracked 17,826,855 research outputs across all sources so far. Compared to these this one has done well and is in the 76th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 497 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.4. This one has gotten more attention than average, scoring higher than 64% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 271,995 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 75% of its contemporaries.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them