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.
The project aims at providing new knowledge and technological solutions to plant infections caused by fungal pathogens and responsible for the most devastating crop diseases. Botrytis cinerea is one of the most important necrotrophic fungus, which causes gray mold disease in more than 200 plant species, including many economically important crops. The ability of host plants to resist to Botrytis can be determined by the composition and structure of the cell wall (CW) and in particular of pectin. Upon cuticle breaking, pectin is early disassembled by pectinases to assist the action of other cell wall degrading enzymes. The pectic polysaccharide homogalacturonan (HG) is the major component of the primary walls of dicot plants. HG is synthesized in the Golgi and secreted in a highly methyl esterified form in the CW. In this compartment, PMEs remove methylesters producing polyanionic HG, methanol (MeOH) and protons. Despite the existing knowledge on PMEs activity during plant-pathogen interaction, much remains to be discovered about their transcriptional regulation. The molecular factors underlying expression PMEs during pathogen attack are still largely unknown and much remains to be discovered about their transcriptional during pathogenesis. Arabidopsis uses local and strong PME activity in the fight against B. cinerea (Lionetti, 2015; Lionetti et al., 2017). However, the molecular factors triggering this response are currently unknown. This project aims to improve knowledge regarding the activation of PME17 expression. Moreover, discover new signaling factors triggering PME activity upon pathogen infection is also a goal of this project. Finally, although the plant defence hormones JA and ET were indicated as possible modulators of PME activity during pathogen infection the molecular pathway involved remains largely unknown, therefore this project aims to clarify this aspect as well.