Ricerc@Sapienza

Plants have evolved the ability to detect invading microbes by perceiving elicitor, called Pathogen- and Damage-Associated Molecular Patterns (PAMPs and DAMPs), that trigger PAMP-Triggered Immunity (PTI). Activation of defense responses during PTI is costly and, in the absence of pathogen pressure, might reduce fitness. For instance, accumulation of high levels of oligogalacturonides (OGs), a plant DAMP, in Arabidopsis OG-M transgenic plants, leads to severe growth reduction. On the other hand, plants treated with elicitors show increased resistance to fungal infection without constitutive expression of defenses. This resistance is likely due to a ¿primed¿ status, where elicited plants are able to respond more quickly and efficiently to subsequent infections. We have recently identified two Arabidopsis genes that are required for elicitor-induced resistance against fungal infection: LYK2, encoding a LysM-Receptor-like Kinase, and PCaP1, encoding a plasma membrane protein involved in the transport of cations. The molecular mechanism underlying the priming phenomenon is not fully elucidated, though it might involve epigenetic changes. Moreover, the basis of the reduced growth observed in OG-treated plants is not clear. We propose to dissect the signaling pathways involved in OG-induced growth reduction, to identify defense-related genes that undergo priming of their expression upon elicitor pre-treatment and to investigate potential epigenetic changes in these genes, to elucidate the molecular basis of elicitor-induced resistance and of the trade-off between defense and growth in plants.