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Chromatin at the crossroads. Meeting on Signalling to Chromatin Epigenetics
Author(s) -
West Adam G,
van Attikum Haico
Publication year - 2006
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7400834
Subject(s) - chromatin , epigenetics , signalling , biology , genetics , microbiology and biotechnology , histone , dna , gene
![][1] In June 2006, about 90 scientists came together at the Wellcome Trust Conference Centre in Hinxton (near Cambridge, UK), to attend the first European Science Foundation (ESF)–Wellcome Trust Conference on Signalling to Chromatin Epigenetics. This meeting addressed how cellular processes both signal and respond to chromatin. Chromatin is composed of nucleosomes that each comprise 147 base pairs of DNA wrapped around an octamer of two copies of each histone H2A, H2B, H3 and H4. Nucleosomes are folded into higher‐order structures that are stabilized by linker histones. Chromatin structure can be altered by enzymes that post‐translationally modify histones (for example, through phosphorylation, acetylation, methylation or ubiquitination) or by ATP‐driven chromatin‐remodelling complexes that alter nucleosome position and/or composition. The role of chromatin in cellular processes, such as transcription, DNA‐damage repair and cell differentiation, was discussed at the meeting. In this report, we summarize a few of the highlights from the broad range of topics discussed.Histone modifications have an important role in the regulation of gene transcription. L. Mahadevan (Oxford, UK) and co‐workers have studied how a particular set of histone modifications controls the rapid induction of the immediate‐early genes c‐jun and c‐fos . Mahadevan showed that on induction by extracellular signals, the extracellular‐signal‐regulated kinase (ERK) and the mitogen‐ and stress‐activated protein kinase 1/2 (MSK1/2) pathways direct a dynamic turnover of acetylation and phosphorylation marks on histone H3 at these genes (Hazzalin & Mahadevan, 2005). Sequential chromatin immunoprecipitation (ChIP) assays showed that acetylated K9‐phosphorylated S10 (H3K9acS10ph) and trimethylated K4 (H3K4me3) forms of histone H3 co‐exist on the same nucleosomes at the promoter and at the 5′‐coding sequences of these genes when they are transcriptionally active. Intriguingly, H3K9acS10ph is only transiently observed on gene induction, whereas H3K4me3 is present before induction. Mahadevan suggested that H3K4me3 might assist in creating a poised state by … [1]: /embed/graphic-1.gif