RITS was discovered in the fission yeast Schizosaccharomyces pombe, and has been shown to be involved in the initiation and spreading of heterochromatin in the mating-type region and in centromere formation.
[4] The maintenance of heterochromatin regions by RITS complexes has been described as a self-reinforcing feedback loop, in which RITS complexes stably bind the methylated histones of a heterochromatin region using the Chp1 protein and induce co-transcriptional degradation of any nascent messenger RNA (mRNA) transcripts, which are then used as RNA-dependent RNA polymerase substrates to replenish the complement of siRNA molecules to form more RITS complexes.
[7] Heterochromatin formation, but possibly not maintenance, is dependent on the ribonuclease protein dicer, which is used to generate the initial complement of siRNAs.
[8] The relevance of observations from fission yeast mating-type regions and centromeres to mammals is not clear, as some evidence suggests that heterochromatin maintenance in mammalian cells is independent of the components of the RNAi pathway.
[10] The role of RNAi in transcriptional gene silencing in plants has been characterized fairly well, and functions primarily through DNA methylation via the RdDM pathway.