The ascomycete Botrytis cinerea Pers. Fr., classified within the family Sclerotiniaceae, is the agent that causes grey mould disease which infects at least 1400 plant species, including crops of economic importance such as grapes and strawberries. The life cycle of B. cinerea consists of two phases: asexual (anamorph, Botrytis cinerea Pers. Fr.) and sexual (teleomorph, Botryotinia fuckeliana (de Bary) Wetzel). During the XVI International Symposium dedicated to the Botrytis fungus, which was held in Bari in June 2013, the scientific community unanimously decided to assign the most widely used name of the asexual form, Botrytis, to this genus of fungi. However, in the literature, we continue to find articles referring to both morphic stages. In this review, we take stock of the genes and metabolites reported for both morphic forms of B. cinerea between January 2015 and October 2022.

Botrytis pseudocinerea is a cryptic fungal species, sympatric with the notorious plant pathogen Botrytis cinerea, yet possessing distinct ecological traits including intrinsic fungicide resistance. Despite this advantage, B. pseudocinerea rarely dominates agricultural ecosystems, presenting an ecological paradox. This study resolves this paradox by defining the unique pathogenic identity of B. pseudocinerea isolate VD165. We demonstrate that VD165 exhibits superior vegetative growth and stress tolerance compared to B. cinerea B05.10, coupled with heightened virulence on solanaceous hosts (tomato, tobacco) but reduced virulence on grape. A comprehensive bio-guided chemical investigation reveals a fundamental metabolic schism: the constitutive and infection-induced upregulation of botcinin polyketides (via Bcboa6/Bcboa9) contrasted with the complete functional loss of the botrydial sesquiterpene pathway. This loss is biochemically confirmed by the significant accumulation of the upstream precursor mevalonolactone. This chemotype, loss of botrydial and compensatory super-activation of botcinins, phenocopies B. cinerea ΔBcbot2 mutants, establishing B. pseudocinerea as a "natural knockout" model that validates the inverse regulation of these major toxin families. We propose that this "evolution by subtraction" is a lineage-specific adaptation shared with the sister species B. fabae, driving host specialization and defining the ecological niche of B. pseudocinerea., This work was supported by the MICIU/AEI under Grant PID-2021-122899 OB-C21 (10.13039/501100011033) and by ERDF/EU., Peer reviewed