Plant Molecular Biology 43: 261–273, 2000.
M.A. Matzke and A.J.M. Matzke (Eds.), Plant Gene Silencing.
© 2000 Kluwer Academic Publishers. Printed in the Netherlands.
RNA degradation and models for post-transcriptional gene silencing
Frederick Meins, Jr.
Friedrich Miescher Institute, A Branch of the Novartis Research Foundation, Postfach 2543, 4002 Basel,
Switzerland (e-mail: email@example.com)
Key words: antisense RNA, double-stranded RNA, epigenetic modiﬁcations, pattern formation, positive autoregu-
lation, post-transcriptional gene silencing, RNA interference, RNA stability, systemic signals
Post-transcriptional gene silencing (PTGS) is a form of stable but potentially reversible epigenetic modiﬁcation,
which frequently occurs in transgenic plants. The interaction in trans of genes with similar transcribed sequences
results in sequence-speciﬁc degradation of RNAs derived from the genes involved. Highly expressed single-copy
loci, transcribed inverted repeats, and poorly transcribed complex loci can act as sources of signals that trigger
PTGS. In some cases, mobile, sequence-speciﬁc silencing signals can move from cell to cell or even over long
distances in the plant. Several current models hold that silencing signals are ‘aberrant’ RNAs (aRNA), which
differ in some way from normal mRNAs. The most likely candidates are small antisense RNAs (asRNA) and
double-stranded RNAs (dsRNA). Direct evidence that these or other aRNAs found in silent tissues can induce
PTGS is still lacking. Most current models assume that silencing signals interact with target RNAs in a sequence-
speciﬁc fashion. This results in degradation, usually in the cytoplasm, by exonucleolytic as well as endonucleolytic
pathways, which are not necessarily PTGS-speciﬁc. Biochemical-switch models hold that the silent state is main-
tained by a positive auto-regulatory loop. One possibility is that concentrations of hypothetical silencing signals
above a critical threshold trigger their own production by self-replication, by degradation of target RNAs, or by a
combination of both mechanisms. These models can account for the stability, reversibility and multiplicity of silent
states; the strong inﬂuence of transcription rate of target genes on the incidence and stability of silencing, and the
ampliﬁcation and systemic propagation of motile silencing signals.
Abbreviations: HDGS, homology-dependent gene silencing; TGA, transcriptional gene sliencing; PTGS, post-
transcriptional gene silencing; SAS, systemic acquired silencing; SIP, silencing-induced principle; IR, inverted
repeat; aRNA, aberrant RNA; asRNA, antisense RNA; dsRNA, double-stranded RNA; RdRP, RNA-dependent
RNA polymerase; RNAi, RNA interference; dsRNase, double-stranded RNA-speciﬁc RNase; ssRNase, single-
stranded RNA-speciﬁc RNase.
Problems worthy of attack prove their worth by hitting
P. Hein (1966)
Interactions between transgenes and host genes of
similar sequence in plants frequently lead to trans-
inactivation of expression at the mRNA level. Once
established the inactive (silent) state is stable: it can
persist in vegetatively growing plants and, in some
cases, is meiotically transmitted to progeny. Neverthe-
less, silenced genes can return to an expressed state
indicating that the stable changes are potentially re-
versible and, hence, a form of epigenetic modiﬁcation
It is now recognized that this phenomenon, called
homology-dependent gene silencing (HDGS) (Meyer
and Saedler, 1996), occurs generally in plants and is
similar to certain types of gene silencing described