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Post-transcriptional gene silencing in plants

Laboratoire de Biologie Cellulaire, INRA, Versailles 78026, France

View larger version (31K): [in a new window]   Fig. 1. Evidence for a systemic silencing signal and for a maintenance step in PTGS. (A) Wild-type plants (wt) do not undergo PTGS after grafting onto silenced transgenic plants. (B) Transgenic plants that do not spontaneously undergo PTGS (class I) undergo PTGS after grafting onto silenced transgenic plants but do not maintain silencing after elimination of the silenced rootstock. (C) Non-silenced transgenic plants derived from lines that can spontaneously undergo PTGS (class II) undergo PTGS after grafting onto silenced transgenic plants and maintain silencing after elimination of the silenced rootstock. (D) Non-transgenic plants that express an endogenous gene at high level owing to metabolic derepression (class III) undergo PTGS after grafting onto silenced transgenic plants but do not maintain silencing after elimination of the silenced rootstock.

View larger version (19K): [in a new window]   Fig. 2. A model for PTGS in plants. Transgene loci arranged as inverted repeats or viruses can directly produce dsRNA. Like dsRNA injected in animals, they can be cut by dsRNase (e.g. the DICER enzyme of Drosophila), thus generating siRNAs. The latter could target mRNA to an RNA-degradation complex (named RISC in Drosophila). Transgene loci carrying a single copy expressed at high level could transcribe abRNAs owing to changes in chromatin structure induced by DDM1. These abRNAs could be used as templates by an RdRP (SGS2/SDE1) to synthesize dsRNAs. This RdRP could be helped by two proteins of unknown function (SGS3 and AGO1) and an RNA helicase (SDE3), which are not required for PTGS induced by IR transgene loci that directly produce dsRNA. The dsRNAs could also induce methylation of transgene DNA (involving MET1), thus reinforcing its ability to produce abRNAs.

View larger version (93K): [in a new window]   Fig. 3. PTGS-deficient mutants are hypersusceptible to infection by CMV. Non-infected PTGS-deficient sgs mutants of Arabidopsis (C) grow as non-infected wild-type plants (A), whereas disease symptoms are much more pronounced in CMV-infected mutants (D) compared with CMV-infected wild-type plants (B). Infected mutants have very small stems, are completely sterile and eventually die, whereas infected wild-type plants develop stems with elongated internodes and are still able to form seeds. The difference in symptom severity caused by CMV infection is due to an average fivefold overaccumulation of viral RNA in the mutants.

View larger version (72K): [in a new window]   Fig. 4. Inhibition of PTGS by viruses. Introduction of a 35S-NiR transgene into tobacco can trigger PTGS of endogenous NiR genes, which leads to growth inhibition and leaf chlorosis (A). Infection by viruses such as CMV or TEV (a potyvirus) inhibits PTGS and restores the growth of plants (B).

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