Establishment of histone h3 methylation on the inactive X chromosome requires transient recruitment of Eed-Enx1 polycomb group complexes.

By Jose Silva, W. Mak, I. Zvetkova, Ruth Appanah, T. Nesterova, Zoe Webster, A. Peters, T. Jenuwein, A. Otte, N. Brockdorff. Developmental Cell, 2003

692 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/97ff7e4f6696e7cb0204916b8f069f3eef97a66b

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Citations in the corpus

Partitioning and plasticity of repressive histone methylation states in mammalian chromatin. (2003, neutral): “Additional quantitation by real-time PCR chromosome (Plath et al., 2003; Silva et al., 2003).”
Child health, developmental plasticity, and epigenetic programming. (2011, background): “(312) have shown that the recruitment of PRCs to the Xi occurs in both imprinted and random X-inactivation, which occurs in the embryo proper.”
Whole-genome mapping of histone H3 Lys4 and 27 trimethylations reveals distinct genomic compartments in human embryonic stem cells. (2007, background): “In mammals, histone H3 Lys9 dimethylation and Lys27 trimethylation (H3K27me3) mark the heterochromatic and inactive X chromosome (Boggs et al., 2002; Peters et al., 2002; Plath et al., 2003; Silva et al., 2003 ).”
The Xist lncRNA exploits three-dimensional genome architecture to spread across the X-chromosome (2013, background): “Xist initiates X-chromosome inactivation (XCI) by spreading in cis across the future inactive X chromosome (20, 21), recruiting polycomb repressive complex 2 (PRC2) (14, 22, 23), and forming a transcriptionally silent nuclear compartment (24, 25) enriched for repressive chromatin modifications inclu”
The diverse functions of histone lysine methylation (2005, background): “Based on the analyses of entire chromosomes as well as individual genes, it seems that trimethyl-H3-K27 is enriched at silenced homeotic genes, the inactive X-chromosome and imprinted genes 64,72,73,76,77 .”
Control of developmental regulators by Polycomb in human embryonic stem cells. (2006, background): “As a critical subunit of the PRC2 complex, Suz12 has widely accepted roles in euchromatic gene silencing and dosage compensation, where Suz12 and H3K27me3 are transiently enriched on the Xi during Xinactivation (Plath et al., 2003; Silva et al., 2003; de la Cruz et al., 2005).”
Directly reprogrammed fibroblasts show global epigenetic remodeling and widespread tissue contribution. (2007, neutral): “The coincidence of Ezh2 accumulation and H3me3K27 enrichment on the Xi are hallmarks only of early phases of X inactivation (Plath et al., 2003; Silva et al., 2003 ).”
Xist nucleates local protein gradients to propagate silencing across the X chromosome (2021, background): “RYBP-PRC1 complexes mediate H2A ubiquitylation at polycomb target sites independently of PRC2 and H3K27me3.”
JHDM2A, a JmjC-containing H3K9 demethylase, facilitates transcription activation by androgen receptor. (2006, background): “In addition, tri-methyl-H3K27, which is associated with the inactive X chromosome in the trophoblast stem (TS) cells, disap-pears during TS cell differentiation (Plath et al., 2003; Silva et al., 2003).”
The profile of repeat‐associated histone lysine methylation states in the mouse epigenome (2005, background): “By contrast, H3-K27 trimethylation is enriched at the inactive X chromosome (Plath et al, 2003; Silva et al, 2003; Kohlmaier et al, 2004).”
Structural basis for specific binding of Polycomb chromodomain to histone H3 methylated at Lys 27. (2003, background): “2002) as well as with the inactive X chromosome (Plath et al. 2003; Silva et al. 2003).”
Promotion of Reprogramming to Ground State Pluripotency by Signal Inhibition (2008, background): “Immunostaining against the silent chromatin mark trimethyl H3-K27 (me3H3K27) readily identifies the inactive X chromosome [16].”
An epigenetic road map for histone lysine methylation (2003, background): “…the inactive X chromosome (Xi) (Boggs et al., 2002; Peters et al., 2002; Heard et al., 2001; Mermoud et al., 2002), but H3K27 tri-methylation might also be a prominent, if not the major, mark (Silva et al., 2003; Plath et al., 2003) (A. H. Peters, S. Kubicek, L. Perez-Burgos et al., unpublished).”