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Background  Germline nuclear RNAi in  C. elegans  is a transgenerational gene-silencing pathway that leads to H3K9 trimethylation (H3K9me3) and transcriptional silencing at the target genes. H3K9me3 induced by either exogenous double-stranded RNA (dsRNA) or endogenous siRNA (endo-siRNA) is highly specific to the target loci and transgenerationally heritable. Despite these features, the role of H3K9me3 in siRNA-mediated transcriptional silencing and inheritance of the silencing state at native target genes is unclear. In this study, we took combined genetic and whole-genome approaches to address this question.    Results  Here we demonstrate that siRNA-mediated H3K9me3 requires combined activities of three H3K9 histone methyltransferases: MET-2, SET-25, and SET-32.  set - 32  single,  met - 2 set - 25  double, and  met - 2 set - 25;set - 32  triple mutant adult animals all exhibit prominent reductions in H3K9me3 throughout the genome, with  met - 2 set - 25;set - 32  mutant worms losing all detectable H3K9me3 signals. Surprisingly, loss of high-magnitude H3K9me3 at the native nuclear RNAi targets has no effect on the transcriptional silencing state. In addition, the exogenous dsRNA-induced transcriptional silencing and heritable RNAi at  oma - 1 , a well-established nuclear RNAi reporter gene, are completely resistant to the loss of H3K9me3.    Conclusions  Nuclear RNAi-mediated H3K9me3 in  C. elegans  requires multiple histone methyltransferases, including MET-2, SET-25, and SET-32. H3K9me3 is not essential for dsRNA-induced heritable RNAi or the maintenance of endo-siRNA-mediated transcriptional silencing in  C. elegans . We propose that siRNA-mediated transcriptional silencing in  C. elegans  can be maintained by an H3K9me3-independent mechanism.    Electronic supplementary material  The online version of this article (doi:10.1186/s13072-017-0114-8) contains supplementary material, which is available to authorized users.

epigenetics and chromatin

Decoupling the downstream effects of germline nuclear RNAi reveals that H3K9me3 is dispensable for heritable RNAi and the maintenance of endogenous siRNA-mediated transcriptional silencing in Caenorhabditis elegans