Supplementary Table S6. Distribution of all the putative PKS described by Suarez et al. in 2024 among other Fungi

Supplementary Table S6. Functional protein annotation from B. deweyae proteins identified in the contigs (NW_024066275.1-NW_024066283.1 absent in B. cinerea B05.10

Supplementary Table S7. Botrytis deweyae protein distribution, indetified in contig NW_024066275.1, in other Botrytis species

Supplementary Table S2. Distribution of the BcStc gamily among the Botrytis genera with NCBI ID

Supplementary Table S9. Top 4 Homologous protein to BdPKS24 in other fungal species

Supplementary Table S11. Top 55 homologous proteins to BdPKS26 in other fungal species

Supplementary Table S8. Top 51 homologous protein to BdPKS23 in other fungal species

Supplementary Table S3. BUSCO analysis for B. deweyae B1 and B. cinerea B05.10

Supplementary Table S2. B. cinerea genome annotation with COGs, GOs, E.C., KEGG, CAZy, BiGG and Pfam databases

Supplementary Table S5. B. deweyae B1 contigs distribution among B. cinerea B05.10 chromosomes

Supplementary Table S2. BGCs originated by antiSMASH fungal version from B. cinerea B05.10 genome

Supplementary Table S7. Top 18 homologous protein to BdPKS22 in other fungal species

Supplementary Table S5. PKS domains of all the putative PKS identified in B. cinerea and B. deweyae.

Supplementary Table S10. Top 25 homologous proteins to BdPKS25 in other fungal species

B. deweyae genome annotation with COGs, GOs, E.C., KEGG, CAZy, BiGG and Pfam databases

Supplementary Table S1. List of oligos used in this study

Supplementary Table S3. Homologous protein to BcStc4 protein identified in other fungus by Blastp

Supplementary Table S4. The top 55 homologous protein to XP 038807933

Supplementary Table S8. B. cinerea B05.10 and B. deweyae B1 protein distribution according to the annotation with KEGG, COGs, CAZy, TCDB and E.C. database

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.

BGCs originated by antiSMASH fungal version from B. deweyae B1 genome

Supplementary Table S3. Orthologous gene identification by blastp in B. deweyae B1 of the 24 most studied virulence factors reported by Nicholas Cheung et al. in 2020.

Supplementary Table S4. Oligos used for Rt-PCR analysis of Bcbot2 gene.

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