Ricerc@Sapienza

The plant cell wall (CW) is the foremost interface where interactions between plants and fungi take place. Fungal pathogens use CW degrading enzymes to digest plant CWs, gaining access to host tissues and causing extensive devastation. The plant Pectin Methylesterases (PMEs) emerge as critical factors for the outcome of plant-fungus interaction. AtPME17 isoform is strongly upregulated in response to several pathogens. AtPME17 is a putative A. thaliana PME highly induced in response to Botrytis cinerea. AtPME17 strongly contributes to the pathogen induced PME activity and resistance against B. cinerea. AtPME17 promoter shows the presence of stress-responsive elements as well as of elements responsive to defense hormones such as jasmonic acid (JA), salicylic acid (SA), abscisic acid (ABA), and ethylene (ET). The expression of AtPME17 is driven by different defense hormones. In particular, the AtPME17 expression is altered in the hormonal mutants ein2-5, jar-1, sid2-2, and aba2-3 mutants when challenged with B. cinerea indicating that ABA, JA, SA, and ET signaling networks contribute to trigger AtPME17 expression during infection. Although these genetic evidences the molecular pathway involved in the activation of AtPME17 expression remains still largely unknown. Using biological and biochemical approaches this research foresees to unveil the molecular factors triggering PME17 expression in Arabidopsis during Botrytis infection. This research will provide new insights about plant molecular mechanisms contrasting fungal penetration and diffusion, useful to develop crop varieties with a durable resistance to necrotrophs.