It has been known for more than a decade that increasing the gene copy numb
er does not necessarily lead to increased gene activity. Plants have develo
ped efficient mechanisms such as post-transcriptional gene silencing (PTGS)
to regulate abnormal gene expression in a sequence-specific fashion. PTGS
of (trans)genes can be inhibited by non-homologous viruses, and PTGS-impair
ed mutants can be hypersensitive to such viruses, indicating that in plants
this mechanism is triggered to protect against viral invasion. Genetic ana
lysis of a related phenomenon, quelling, in Neurospora has led to the ident
ification of two genes encoding proteins that share homologies with RNA-dep
endent RNA polymerases and with DNA helicases. This finding reinforces prev
ious models in which PTGS involves RNA molecules complementary to the RNA s
pecies targeted for degradation. Insight into the mechanisms of PTGS may al
so be obtained in other distant organisms such as Caenorhabditis elegans in
which a related phenomenon, RNA interference, has been genetically studied
, leading to the identification of two genes encoding proteins sharing homo
logies with a translation factor and an RNase D.