The euchromatic and heterochromatic landscapes are shaped by antagonizing effects of transcription on H2A.Z deposition

• Published in: PLoS genetics Vol. 5; no. 10; p. e1000687
• Main Authors: Hardy, Sara, Jacques, Pierre-Etienne, Gévry, Nicolas, Forest, Audrey, Fortin, Marie-Eve, Laflamme, Liette, Gaudreau, Luc, Robert, François
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 01.10.2009; Public Library of Science (PLoS)
• Subjects: Cancer; Cell Biology/Gene Expression; Cell Line, Tumor; Chromatin; DNA repair; Embryonic stem cells; Euchromatin; Experiments; Gene expression; Genetic aspects; Genetics and Genomics/Epigenetics; Genetics and Genomics/Functional Genomics; Genetics and Genomics/Gene Expression; Genomes; Heterochromatin; Histones - genetics; Histones - metabolism; Humans; Insects; Medical research; Molecular Biology/Chromatin Structure; Molecular Biology/Histone Modification; Molecular Biology/Transcription Elongation; Molecular Biology/Transcription Initiation and Activation; Physiological aspects; Promoter Regions, Genetic; RNA polymerase; RNA Polymerase II - metabolism; Stem cells; Structure; Transcription, Genetic; Yeast; Canada
• ISSN: 1553-7404; 1553-7390; 1553-7404
• DOI: 10.1371/journal.pgen.1000687

A role for variant histone H2A.Z in gene expression is now well established but little is known about the mechanisms by which it operates. Using a combination of ChIP-chip, knockdown and expression profiling experiments, we show that upon gene induction, human H2A.Z associates with gene promoters and helps in recruiting the transcriptional machinery. Surprisingly, we also found that H2A.Z is randomly incorporated in the genome at low levels and that active transcription antagonizes this incorporation in transcribed regions. After cessation of transcription, random H2A.Z quickly reappears on genes, demonstrating that this incorporation utilizes an active mechanism. Within facultative heterochromatin, we observe a hyper accumulation of the variant histone, which might be due to the lack of transcription in these regions. These results show how chromatin structure and transcription can antagonize each other, therefore shaping chromatin and controlling gene expression.