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Small RNA-directed control of the plant and animal innate immune responses

Final Report Summary - SILENCING & IMMUNITY (Small RNA-directed control of the plant and animal innate immune responses)

Post-Transcriptional Gene Silencing (PTGS) is a conserved mechanism of gene regulation that has been initially characterized in antiviral resistance in plants. More recently, this mechanism was shown to contribute to resistance against bacterial, fungal and oomycete plant pathogens. As a counter-defense mechanism, viral and bacterial phytopathogens produce toxins, referred to as pathogen effectors, which suppress PTGS. For instance, the Pseudomonas syringae pv. tomato strain DC3000 (Pto DC3000) was shown to inject several bacterial effectors within plant cells to suppress PTGS, although the mechanism involved in this process remain ill-defined. We have recently identified the mode of action of one of these Pto DC3000 effectors. Interestingly, we have provided evidence that this strategy is likely widespread and have demonstrated experimentally that one effector from a human pathogenic bacterium can use an analogous strategy. These findings indicate that human bacterial pathogens have evolved to suppress RNA silencing, which has not yet been reported so far. Furthermore, we have demonstrated that DNA methylation negatively regulates the plant immune response by repressing the basal expression of immune -responsive genes. Importantly, a release of transcriptional gene silencing was observed presumably as a consequence of the transcriptional repression of RNA-directed DNA methylation (RdDM) factors, which was found to require potentially a family of known defense-related transcription factors. In addition, we provided compelling evidence that active DNA demethylation is essential to ensure a proper transcriptional activation of defense-related genes, which include functionally relevant disease resistance genes. This regulatory mechanism involves the constitutive demethylation of transposable element boundaries, which presumably facilitate the accessibility of defense-related transcription factors onto the chromatin. Finally, we have identified Pto DC3000 effectors that interfere with the expression of endogenous and exogenous RdDM targets, although the detailed mode of action of these effectors remain to be elucidated.