Abstract
The knowledge about the molecular mechanisms underlying Botrytis cinerea attack on susceptible hosts has expanded greatly in the last years. While many details are still missing, it is possible now to generate a higher resolution image of the molecular patterns that regulate pathogenic development of this broad host range necrotroph. Several decades of molecular research, including the complete genome sequencing and analyses of two B. cinerea strains, have culminated into a working model outlining the molecular strategy used by B. cinerea in the infection process. It is now apparent that a complex signalling network regulates secretion of a large set of proteins and phytotoxic secondary metabolites, which are necessary for progression of the infection from the early to late stages. Furthermore, manipulation of the plant hyper-sensitive response (HR), a form of programmed cell death (PCD), has been proposed to play a central role in the pathogenic strategy of B. cinerea. Although the molecular details of this aspect are largely uncharacterized, it is possible that some of the secreted proteins and metabolites function as effectors that target the PCD machinery. The virulence factors that have been revealed in these various categories and in others are reviewed in this chapter, with special emphasis on secreted proteins and PCD.
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