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RNA Interference and Gene Silencing: History and Overview

th mutated rde-2 or mut-7 genes exhibit defective RNAi, but interestingly, they also demonstrate increased levels of transposon activity. Thus, silencing of transposons appears to occur by a mechanism related to RNAi and PTGS. Although the rde-2 gene product has not yet been identified, the mut-7 gene encodes a protein with homology to the nuclease domains of RNase D and a protein implicated in Werner syndrome (a rapid aging disease) in humans (1, 3, 17, 18, 31). Perhaps this protein is a candidate for the nuclease activity required for target RNA degradation.

PTGS Has Ancient Roots
Discoveries from both genetic and biochemical approaches point to the fact that PTGS has deep evolutionary roots. Proposals have been put forth that PTGS evolved as a defense mechanism against transposons or RNA viruses, perhaps before plants and animals diverged (1, 3, 17, 18).

Interestingly, it was noted by many researchers that disruption of genes required for RNAi often causes severe developmental defects. This observation suggested a link between RNAi and at least one developmental pathway.

A group of small RNA molecules, known as small temporal RNAs (stRNAs), regulates C. elegans developmental timing through translational repression of target transcripts. Research indicates that the C. elegans lin-4 and let-7 stRNAs are generated from 70-nt transcripts following the folding of these longer tran
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