EFFECTOR TRIGGERED IMMUNITY

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Abstract

In plants, the Leucine Rich Receptor proteins (NS-LRR and LRR-RK) are at the basis of ETI and HR response to pathogen elicitors. It was shown that swapping the domains that trigger Effector Triggered Immunity or Hypersensitive Response made possible the modulation of plant response to pathogen attack.Most pathogenic and nonpathogenic/symbiotic bacteria use type III secretion system to inject into host cells, effector proteins promoting virulence or symbiosis (Chisholm et al., 2006; Xin et al., 2012).The second evasion strategy is exemplified by the Pseudomonads AprA protein, which digests monomeric flagellin that hampers plants and vertebrates recognition. Finally, the last evasion mechanism is based on MAMP modification. Indeed, pathogen PRR recognition triggers defence mechanisms that create a pressure of selection on bacteria. Some successful microbes such as plant pathogens Ralstonia solanacearum or Xanthomonas campestri pv campestris B186 (XccB186) have evolved to evade TLR5 or FLS2 recognition by mutating their flagellin-encoding genes. Since these bacteria require motility for colonization and persistence in their hosts, sequences contain not only changes that permit PRR evasion, but also compensatory mutations that restore flagellin polymerization.Considering the important role of PRR in innate immunity and the possibility of a PRR transfer to crop that confers broad-spectrum resistance to several bacterial pathogens, we sought to enhance plant recognition capabilities to express the TLR5 in Arabidopsis thaliana.

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  • P. Poltronieri; A. Santino; F. Francocci ; B. Reca ; A. Brutus

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Anno di pubblicazione

2015

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