Human CpG binding protein interacts with MLL1, MLL2 and hSet1 and regulates Hox gene expression

Ansari, Khairul I.; Mishra, Bibhu Prasad; Mandal, Subhrangsu S.

doi:10.1016/j.bbagrm.2007.11.006

Cited by 59 publications

(84 citation statements)

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“…Indeed, it is widely considered that the enrichment of CpGs at promoters is a vertebratespecific phenomenon that requires DNA methylation (Duncan and Miller 1980;Gardiner-Garden and Frommer 1987;Cooper and Krawczak 1989;Ehrlich et al 1990;Antequera and Bird 1999;Caiafa and Zampieri 2005;Illingworth and Bird 2009;Turner et al 2010;Deaton and Bird 2011). In mammals, nonmethylated CpGs are associated with active promoter chromatin features and bound by CXXC1 (CFP1), which is part of a SETD1A complex that catalyzes methylation of H3K4 (Lee and Skalnik 2005;Ansari et al 2008;Butler et al 2008;Tate et al 2010;Thomson et al 2010;Xu Ó 2014 Chen et al This article, published (Simonet et al 2007;Li and Kelly 2011), suggesting a possible similarity of function.…”

Section: [Supplemental Materials Is Available For This Article]mentioning

confidence: 99%

Extreme HOT regions are CpG-dense promoters in C. elegans and humans

et al. 2014

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Most vertebrate promoters lie in unmethylated CpG-dense islands, whereas methylation of the more sparsely distributed CpGs in the remainder of the genome is thought to contribute to transcriptional repression. Nonmethylated CG dinucleotides are recognized by CXXC finger protein 1 (CXXC1, also known as CFP1), which recruits SETD1A (also known as Set1) methyltransferase for trimethylation of histone H3 lysine 4, an active promoter mark. Genomic regions enriched for CpGs are thought to be either absent or irrelevant in invertebrates that lack DNA methylation, such as C. elegans; however, a CXXC1 ortholog (CFP-1) is present. Here we demonstrate that C. elegans CFP-1 targets promoters with high CpG density, and these promoters are marked by high levels of H3K4me3. Furthermore, as for mammalian promoters, high CpG content is associated with nucleosome depletion irrespective of transcriptional activity. We further show that highly occupied target (HOT) regions identified by the binding of a large number of transcription factors are CpG-rich promoters in C. elegans and human genomes, suggesting that the unusually high factor association at HOT regions may be a consequence of CpG-linked chromatin accessibility. Our results indicate that nonmethylated CpG-dense sequence is a conserved genomic signal that promotes an open chromatin state, targeting by a CXXC1 ortholog, and H3K4me3 modification in both C. elegans and human genomes.[Supplemental material is available for this article.]Transcription is regulated through functional elements in the genome such as promoters and enhancers. Identifying these genomic elements, many of which are recognized by transcription factors (TFs), is a necessary first step in their functional analysis. Toward this goal, the modENCODE and ENCODE Projects have used chromatin immunoprecipitation (ChIP) to map the binding sites for a large number of TFs in C. elegans, Drosophila, and humans

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Section: [Supplemental Materials Is Available For This Article]mentioning

confidence: 99%

Extreme HOT regions are CpG-dense promoters in C. elegans and humans

et al. 2014

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“…Unmethylated CpG dinucleotides within CpG islands (reviewed in ref. 55) may primarily recruit CXXC motif-containing proteins, including the H3K4 methyltransferase MLL1 (56) and CGBP/ Cfp1, which associates with H3K4 methyltransferases (57,58). DNA binding by Cfp1 has recently been shown to restrict Setd1A and H3K4me3 to euchromatic nonmethylated CpG regions (59).…”

Section: Cotargeting Of H3k4 Trimethylation and Dynamic Acetylation Tmentioning

confidence: 99%

Dynamic acetylation of all lysine-4 trimethylated histone H3 is evolutionarily conserved and mediated by p300/CBP

Crump

Hazzalin

Bowers

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

101

111

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Histone modifications are reported to show different behaviors, associations, and functions in different genomic niches and organisms. We show here that rapid, continuous turnover of acetylation specifically targeted to all K4-trimethylated H3 tails (H3K4me3), but not to bulk histone H3 or H3 carrying other methylated lysines, is a common uniform characteristic of chromatin biology in higher eukaryotes, being precisely conserved in human, mouse, and Drosophila. Furthermore, dynamic acetylation targeted to H3K4me3 is mediated by the same lysine acetyltransferase, p300/cAMP response element binding (CREB)-binding protein (CBP), in both mouse and fly cells. RNA interference or chemical inhibition of p300/CBP using a newly discovered small molecule inhibitor, C646, blocks dynamic acetylation of H3K4me3 globally in mouse and fly cells, and locally across the promoter and start-site of inducible genes in the mouse, thereby disrupting RNA polymerase II association and the activation of these genes. Thus, rapid dynamic acetylation of all H3K4me3 mediated by p300/CBP is a general, evolutionarily conserved phenomenon playing an essential role in the induction of immediate-early (IE) genes. These studies indicate a more global function of p300/CBP in mediating rapid turnover of acetylation of all H3K4me3 across the nuclei of higher eukaryotes, rather than a tight promoter-restricted function targeted by complex formation with specific transcription factors.histone acetylation turnover | Trichostatin A | p300/CBP inhibitor

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“…They exist as distinct multiprotein complexes inside cells with several common subunits including ASH2, WDR5, RBBP5, CGBP, and DPY30 (Lee & Skalnik 2005, Crawford & Hess 2006, Dou et al 2006, Ansari et al 2008, Trievel & Shilatifard 2009. Recently, we have demonstrated that MLL1 and H3K4 trimethylation have distinct dynamics during cell cycle progression and play critical roles in gene activation (Ansari et al 2008, 2009a,b,c, Mishra et al 2009). Knockdown of MLL1 results in cell cycle arrest at G2/M phase, suggesting its critical role in cell cycle progression (Takeda et al 2006, Ansari et al 2009a.…”

Section: Introductionmentioning

confidence: 99%

HOXC10 is overexpressed in breast cancer and transcriptionally regulated by estrogen via involvement of histone methylases MLL3 and MLL4

Ansari¹,

Hussain²,

Kasiri³

et al. 2011

Journal of Molecular Endocrinology

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HOXC10 is a critical player in the development of spinal cord, formation of neurons, and associated with human leukemia. We found that HOXC10 is overexpressed in breast cancer and transcriptionally regulated by estrogen (17b-estradiol, E 2 ). The HOXC10 promoter contains several estrogen response elements (ERE1-7, half-sites). A luciferase-based reporter assay showed that ERE1 and ERE6 of HOXC10 promoter are E 2 responsive. ERa and ERb play critical roles in E 2 -mediated activation of HOXC10. Knockdown of ERa and ERb downregulated E 2 -induced HOXC10 expression. ERa and ERb bind to ERE1 and ERE6 regions in an E 2 -dependent manner. Additionally, knockdown of histone methylases MLL3 and MLL4 (but not MLL1 and MLL2) diminished E 2 -induced expression of HOXC10. MLL3 and MLL4 were bound to the ERE1 and ERE6 regions of HOXC10 promoter in an E 2 -dependent manner. Overall, we demonstrated that HOXC10 is overexpressed in breast cancer, and it is an E 2 -responsive gene. Histone methylases MLL3 and MLL4, along with ERs, regulate HOXC10 gene expression in the presence of E 2 .

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Human CpG binding protein interacts with MLL1, MLL2 and hSet1 and regulates Hox gene expression

Cited by 59 publications

References 50 publications

Extreme HOT regions are CpG-dense promoters in C. elegans and humans

Extreme HOT regions are CpG-dense promoters in C. elegans and humans

Dynamic acetylation of all lysine-4 trimethylated histone H3 is evolutionarily conserved and mediated by p300/CBP

HOXC10 is overexpressed in breast cancer and transcriptionally regulated by estrogen via involvement of histone methylases MLL3 and MLL4

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