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First published online September 12, 2006
doi: 10.1242/10.1242/dev.02584
1 Department of Biology, Indiana University, Bloomington, IN 47405, USA.
2 Department of Biochemistry, Purdue Cancer Center, Purdue University, West
Lafayette, IN 47907, USA.
3 Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer
Center, University of North Carolina at Chapel Hill, NC 27599, USA.
4 Department of Genetics, Yale University School of Medicine, New Haven, CT
06520, USA.
Authors for correspondence (e-mail:
lbender{at}indiana.edu;
sstrome{at}indiana.edu)
Accepted 8 August 2006
Germ cell development in C. elegans requires that the X chromosomes be globally silenced during mitosis and early meiosis. We previously found that the nuclear proteins MES-2, MES-3, MES-4 and MES-6 regulate the different chromatin states of autosomes versus X chromosomes and are required for germline viability. Strikingly, the SET-domain protein MES-4 is concentrated on autosomes and excluded from the X chromosomes. Here, we show that MES-4 has histone H3 methyltransferase (HMT) activity in vitro, and is required for histone H3K36 dimethylation in mitotic and early meiotic germline nuclei and early embryos. MES-4 appears unlinked to transcription elongation, thus distinguishing it from other known H3K36 HMTs. Based on microarray analysis, loss of MES-4 leads to derepression of X-linked genes in the germ line. We discuss how an autosomally associated HMT may participate in silencing genes on the X chromosome, in coordination with the direct silencing effects of the other MES proteins.
Key words: C. elegans, MES proteins, Histone methylation, Germ line, X-chromosome silencing
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