Botrytis cinerea, the causal agent of gray mold, is a necrotrophic fungus with a wide range of hosts and is a major post-harvest problem. As opposite to biotrophic fungi, host responses against necrotrophs are not well understood. I am currently investigating the role of known arabidopsis defense mechanisms in restricting the growth of this pathogen. This project takes advantage of the numerous mutants isolated for their altered susceptibility against different kind of pathogens. In particular, my aim is to define what responses are effective against a wide range of pathogens and what are important against one or few microbial species.

Defensins are small antimicrobial polypeptides produced by both animals and plants after microbial infections. While other plant pathogenesis-related proteins (PR1, BGL2, PR5) are induced by salicylic acid (SA), defensin expression is independent on SA but requires jasmonic acid (JA) and ethylene. Some arabidopsis mutants isolated for defective or constitutive expression of PR genes also revealed an altered pattern of expression of the defensin gene PDF1.2, suggesting a cross-talk between the two pathways.

In our lab, a screening for arabidopsis mutants specifically defective in defensin accumulation after infiltration with the fungal toxin fumonisin B1 has been accomplished, and the most promising lines are being characterized. Furthermore, the regulation of different defensin genes is under investigation.

Polygalacturonases (PGs) are among the first cell wall-degrading enzymes secreted by phytopathogenic fungi during the colonization of a plant host. The plant host responds to the infection producing, along with other defense proteins, polygalacturonase-inhibiting proteins (PGIPs) that specifically bind and inhibit fungal PGs. PGIPs are apoplastic leucine-rich repeat (LRR) proteins with high homology with the extracellular domain of several resistance genes and other transmembrane receptors; the solvent-exposed portion of the LRR domain has been shown to determine the specificity of recognition of the ligand. It has been reported that the overexpression of a pear PGIP gene in tomato increased the resistance to a fungal pathogen; moreover, PGIP expression in different species is usually induced by fungal infections, wounding, elicitors and salicylic acid, suggesting a role in the defense response. However, different genes in the same species appear to be differentially regulated and show different specificity.

In order to elucidate the role of these proteins in both pathological and physiological conditions, two arabidopsis genes with high homology with known PGIPs were cloned and their characterization is currently in progress. Analysis of the Atpgip genes expression in wild type and mutant plants, and the effects of their overexpression in transgenic plants will reveal more insights in the role of PGIPs in plant defense against pathogens.