Mutations in another pathway, that of RNA interference (RNAi), produced related results. One way RNAi works is by unleashing the Dicer-2 enzyme to chop strands of RNA into short lengths, which can degrade messenger RNA and prevent gene expression.
Karpen explains that "the RNAi pathway is a sort of immune system against viral DNA and transposons." Transposons are pieces of DNA that can "jump" to different locations in the genome, either directly or by copying themselves, inserting themselves in new sequences where they can cause mutations.
"Short repetitive pieces of DNA that keep copying themselves could conceivably expand and take over the whole genome," says Karpen, "so some balance must be achieved, between the need for replication processes on the one hand and the need to repress or control or regulate those processes on the other."
Since DNA pieces that copy themselves must use RNA intermediates, these can be disabled by RNA interference. Transposons are also silenced by accumulating in the transcriptionally-silent heterochromatin, which Karpen calls "a graveyard of transposons."
While the gene for the Dicer-2 enzyme, dcr-2, is a key player in the RNAi pathway, the RNAi process also targets H3K9 methylation. Sure enough, Karpen and Peng found that Drosophila with mutant dcr-2 genes showed multiple nucleoli and other symptoms of heterochromatin deregulation, just as Su(var)3-9 mutants did.
The road to regulation
One effect of both Su(var)3-9 and RNAi mutations was to increase the amount of extrachromo
Source:DOE/Lawrence Berkeley National Laboratory