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First published online July 27, 2007
In this issue |
Just as chromatin structure influences gene expression, molecules that orchestrate chromatin remodeling can influence cell fate by regulating the transcription of cell-fate specification genes. On p. 2991, Erik Andersen and H. Robert Horvitz investigate the roles of histone methyltransferases (HMTs) in cell-fate specification in Caenorhabditis elegans vulval development. They used RNAi or deletion alleles to systematically probe the phenotypes of all 38 SET-domain-containing HMTs in C. elegans. They found that double mutants in the genes met-1 and met-2 cause ectopic vulva induction, and show that the two HMTs act redundantly to repress the transcription of the EGF gene lin-3, which induces vulval development. This makes met-1 and met-2 so-called synMuv genes, which negatively regulate vulval development. But how do they work? The authors show that MET-1 and MET-2 are homologous to HMTs that methylate histones at H3K36 and H3K9, respectively, and both proteins are required for normal histone trimethylation. They propose a model for the way that these HMTs act with other chromatin-remodeling factors to repress transcription and to inhibit vulval cell fates.
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