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Abstract

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 maintained 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.

Transient Co-Expression of Post-Transcriptional Gene Silencing Suppressors for Increased in Planta Expression of a Recombinant Anthrax Receptor Fusion Protein

“…PTGS has been identified as a plant defense mechanism for aberrant gene expression following agroinfection, such as production of excessive RNA transcripts over a threshold level [43,44]. Several groups have reported that overexpressing a transgene over a certain level causes transgene silencing through activation of PTGS [45–47], including when occurring under CaMV 35S promoter control [48,49]. This evidence supports a theory that PTGS occurs due to the elevated CaMV 35S driven CMG2-Fc expression, regardless of the absence of viral RNAs.…”

Iron deficiency in barley plants: phytosiderophore release, iron translocation, and DNA methylation

“…Although environmental conditions like soil, light, temperature, and microbial activity have been reported to influence Fe uptake and storage (Kokot and Phuong, 1999 ; Lueders and Friedrich, 2000 ; Vansuyt et al, 2000 ), genetic regulatory factors, such as DNA methylation and co-suppression may also play a role (Finnegan et al, 2000 ; Meins, 2000 ). In this regard, cytosine methylation may play an integral role in the regulation of gene expression at both the transcriptional and post-transcriptional levels.…”

Gene Technology for Papaya Ringspot Virus Disease Management

“…Mangrauthia et al [74] suggested that HcPro is an important component which needs to be taken into consideration for the development of PRSV-resistant papaya on the Indian subcontinent. The mechanism of RNA-mediated virus resistance is also referred to as homology dependency resistance to reflect the specific mechanism of posttranscriptional gene silencing (PTGS) [75, 76]. PTGS is the accumulation of 21–25 nucleotide small-interfering RNAs, the sequence-specific degradation of target mRNAs, and the subsequent methylation of target gene sequences.…”