Journal article
Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing
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
EPIGENETICS & CHROMATIN | BMC | Published : 2016
Abstract
BACKGROUND: 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. RESULTS: 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 (S..
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Awarded by Australian National Health and Medical Research Council
Funding Acknowledgements
We thank The Dyson Bequest and The DHB Foundation for philanthropic funding to MEB. This work was supported by grants from the Australian National Health and Medical Research Council ( APP1045936) to MEB. MEB is a Queen Elizabeth II Fellow of the Australian Research Council ( DP1096092). This work was made possible through Victorian State Government Operational Infrastructure Support and Australian National Health and Medical Research Council Research Institute Infrastructure Support Scheme. We also thank Felix Kruegar and Simon Andrews from the Babraham Bioinformatics Department and Emma Whitelaw from La Trobe Institute of Molecular Science for useful advice and Shian Su from WEHI for bionformatic advice.