RNA degradation and models for post-transcriptional gene silencing

Authors
Citation
F. Meins, RNA degradation and models for post-transcriptional gene silencing, PLANT MOL B, 43(2-3), 2000, pp. 261-273
Citations number
120
Language
INGLESE
art.tipo
Review
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PLANT MOLECULAR BIOLOGY
ISSN journal
0167-4412 → ACNP
Volume
43
Issue
2-3
Year of publication
2000
Pages
261 - 273
Database
ISI
SICI code
0167-4412(200006)43:2-3<261:RDAMFP>2.0.ZU;2-K
Abstract
Post-transcriptional gene silencing (PTGS) is a form of stable but potentia lly reversible epigenetic modification, which frequently occurs in transgen ic plants. The interaction in trans of genes with similar transcribed seque nces results in sequence-specific degradation of RNAs derived from the gene s involved. Highly expressed single-copy loci, transcribed inverted repeats , and poorly transcribed complex loci can act as sources of signals that tr igger PTGS. In some cases, mobile, sequence-specific silencing signals can move from cell to cell or even over long distances in the plant. Several cu rrent 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 th at these or other aRNAs found in silent tissues can induce PTGS is still la cking. Most current models assume that silencing signals interact with targ et RNAs in a sequence-specific fashion. This results in degradation, usuall y in the cytoplasm, by exonucleolytic as well as endonucleolytic pathways, which are not necessarily PTGS-specific. Biochemical-switch models hold tha t the silent state is maintained by a positive auto-regulatory loop. One po ssibility is that concentrations of hypothetical silencing signals above a critical threshold trigger their own production by self-replication, by deg radation of target RNAs, or by a combination of both mechanisms. These mode ls can account for the stability, reversibility and multiplicity of silent states; the strong influence of transcription rate of target genes on the i ncidence and stability of silencing, and the amplification and systemic pro pagation of motile silencing signals.