Resumen de Insights into secondary metabolism and pathogenicity of penicillium expansum by genome, transcriptome and functional analysis
A.R. Ballester, M. Marcet Houben, E. Levin, N. Sela, C Selma Lázaro, L. Carmona, M. Wisniewski, S. Droby, Luis González Candelas, T. Gabaldón
Penicillium expansum is the causal agent of the blue mold rot of pome fruit, whereas Penicillium italicum causes blue mound in citrus fruit. Despite their economic importance, the genetic bases of their virulence mechanisms remain unclear. Here, we present the genome sequences of three P. expansum strains and one strain of P. italicum, and their comparison with 24 other Pezizomycotina. As compared with other Penicillia, P. expansum is particularly rich in secondary metabolism clusters, some of which seem to have been acquired by horizontal gene transfer. Patulin is the major mycotoxin produced by P. expansum, whose levels in foods are regulated due to health risks. Two of the three sequenced strains produced patulin under in vitro growth conditions. To further assess its role in pathogenesis, we have constructed knock out mutants for three genes of the patulin biosynthetic gene cluster. All knock out mutants were unable to produce the mycotoxin. However, no differences in virulence on apple fruits were observed among the three sequenced strains neither in the knock out mutants. We further examined fungal gene expression during the apple-P. expansum interaction by dual RNA-Seq. Among the predicted metabolic clusters in P. expansum, 9 of them were expressed during infection. Analysis of expressed genes at 24 hours post inoculation indicate the active growth of the fungus during the initial stage of colonization, the involvement of the exosomes, vesicles that have been related to the delivery of effectors by fungal pathogens, and the expression of putative pathogenicity factors. Our results showed that patulin does not play a role in infection of apple fruit, although we cannot rule out that other secondary metabolites may directly contribute to fungal pathogenicity.
