The CHD3 Remodeler PICKLE Promotes Trimethylation of Histone H3 Lysine 27S

CHD3 proteins are ATP-dependent chromatin remodelers that contribute to repression of developmentally regulated genes in both animal and plant systems. In animals, this repression has been linked to a multiple subunit complex, Mi-2/NuRD, whose constituents include a CHD3 protein, a histone deacetyla...

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Veröffentlicht in:The Journal of biological chemistry 2008-08, Vol.283 (33), p.22637-22648
Hauptverfasser: Zhang, Heng, Rider, Stanley Dean, Henderson, James T., Fountain, Matthew, Chuang, King, Kandachar, Vasundhara, Simons, Alexis, Edenberg, Howard J., Romero-Severson, Jeanne, Muir, William M., Ogas, Joe
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Sprache:eng
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Zusammenfassung:CHD3 proteins are ATP-dependent chromatin remodelers that contribute to repression of developmentally regulated genes in both animal and plant systems. In animals, this repression has been linked to a multiple subunit complex, Mi-2/NuRD, whose constituents include a CHD3 protein, a histone deacetylase, and a methyl-CpG-binding domain protein. In Arabidopsis , PICKLE ( PKL ) codes for a CHD3 protein that acts during germination to repress expression of seed-associated genes. Repression of seed-associated traits is promoted in pkl seedlings by the plant growth regulator gibberellin (GA). We undertook a microarray analysis to determine how PKL and GA act to promote the transition from seed to seedling. We found that PKL and GA act in separate pathways to repress expression of seed-specific genes. Comparison of genomic datasets revealed that PKL -dependent genes are enriched for trimethylation of histone H3 lysine 27 (H3K27me3), a repressive epigenetic mark. Chromatin immunoprecipitation studies demonstrate that PKL promotes H3K27me3 in both germinating seedlings and in adult plants but do not identify a connection between PKL -dependent expression and acetylation levels. Taken together, our analyses illuminate a new pathway by which CHD3 remodelers contribute to repression in eukaryotes.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.M802129200