Sclerotinia sclerotiorum (Lib.) de Bary is a broad host-range fungus that infects an inclusive array of plant species and afflicts significant yield losses globally. Despite being a notorious pathogen, it has an uncomplicated life cycle consisting of either basal infection from myceliogenically germinated sclerotia or aerial infection from ascospores of carpogenically germinated sclerotia. This fungus is unique among necrotrophic pathogens in that it inevitably colonizes aging tissues to initiate an infection, where a saprophytic stage follows the pathogenic phase. The release of cell wall-degrading enzymes, oxalic acid, and effector proteins are considered critical virulence factors necessary for the effective pathogenesis of S. sclerotiorum. Nevertheless, the molecular basis of S. sclerotiorum pathogenesis is still imprecise and remains a topic of continuing research. Previous comprehensive sequencing of the S. sclerotiorum genome has revealed new insights into its genome organization and provided a deeper comprehension of the sophisticated processes involved in its growth, development, and virulence. This review focuses on the genetic and genomic aspects of fungal biology and molecular pathogenicity to summarize current knowledge of the processes utilized by S. sclerotiorum to parasitize its hosts. Understanding the molecular mechanisms regulating the infection process of S. sclerotiorum will contribute to devising strategies for preventing infections caused by this destructive pathogen.
Keywords: cAMP; cell wall degrading enzymes; effectors; life cycle; molecular diagnosis; oxalic acid; pathogenicity; whole genome.