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Molecular and Cellular Biology, July 2009, p. 3700-3709, Vol. 29, No. 13
0270-7306/09/$08.00+0 doi:10.1128/MCB.00018-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Laboratory of Chromatin Biochemistry,1 Electron Microscopy Group,2 Department of Cellular Biochemistry, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, 37077 Göttingen, Germany,3 Institute of Protein Research, Russian Academy of Sciences, 142290 Pushchino, Moscow Region, Russia,4 Department of Proteomics and Signal Transduction, Max Planck Institute for Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany5
Received 6 January 2009/ Returned for modification 6 February 2009/ Accepted 10 April 2009
HIS-24 linker histone and SIR-2.1 deacetylase are involved in chromatin silencing in Caenorhabditis elegans. Depletion of SIR-2.1 results in cytoplasmic retention of HIS-24 in oocytes. However, the molecular working mechanisms of HIS-24 and SIR-2.1 are unclear. We show here a synergistic function of SIR-2.1 and HIS-24 that are together essential for maintenance of the H3K27me3 mark in the germ line of C. elegans. We demonstrate the synthetic effects of the two factors on brood size, embryogenesis, and fertility. SIR-2.1 and HIS-24 associate with the subtelomeric regions but apparently do not interact directly. We report that SIR-2.1 deacetylates H3K9 at subtelomeric regions and suggest that deacetylation of H3K9 is a prerequisite for H3K27 methylation. In turn, we found that HIS-24 specifically interacts with the histone H3 K27 region, when unmodified or in the trimethylated state. Overall, our data indicate that SIR-2.1 and HIS-24 contribute to the propagation of a specialized chromatin state at the subtelomeric regions and elsewhere in the genome.
Published ahead of print on 20 April 2009.
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