Abstract
Botrytis cinerea is one of the most destructive fungal pathogens affecting numerous plant hosts, including many important crop species. As a molecularly under-studied organism, its genome was only sequenced at the beginning of this century and it was recently updated with improved gene annotation and completeness. In this review, we summarize key molecular studies on B. cinerea developmental and pathogenesis processes, specifically on genes studied comprehensively with mutant analysis. Analyses of these studies have unveiled key genes in the biological processes of this pathogen, including hyphal growth, sclerotial formation, conidiation, pathogenicity and melanization. In addition, our synthesis has uncovered gaps in the present knowledge regarding development and virulence mechanisms. We hope this review will serve to enhance the knowledge of the biological mechanisms behind this notorious fungal pathogen.
Highlights
Ascomycete Botrytis cinerea is a fungal pathogen responsible for gray mold diseases.It has a broad host range, affecting many important agricultural crops
Most conidia from bem1 and cdc24 mutants could not germinate and the few germinated ones gradually stopped growing. These results indicate that bud emergence protein 1 (BEM1) and cell division control protein 24 (CDC24) significantly contribute to conidium germination, hyphal growth and host penetration
Many genes involved in the development and pathogenicity of B. cinerea have been characterized
Summary
Ascomycete Botrytis cinerea is a fungal pathogen responsible for gray (or grey) mold diseases It has a broad host range, affecting many important agricultural crops. B. cinerea is a highly successful pathogen due to its flexible infection modes, high reproductive output, wide host range and ability to survive for extended periods as conidia and/or small hardened. Pathogens 2020, 9, 923 output, wide host range and ability to survive for extended periods as conidia and/or small hardened mycelia masses called sclerotia [8]. It is primarily airborne as asexual conidia spores from mature conidiophores as major means of transmission. We hope this review aids in a comprehensive understanding of the molecular mechanisms of the biological processes behind this widespread airborne pathogen
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