Dissecting the genome, secretome, and effectome repertoires of Monilinia spp.: The causal agent of brown rot disease: A comparative analysis

Brown rot is one of the most economically important pomes and stone fruit diseases in the world, incurring significant losses during both pre-and post-harvest phases. The disease is caused by the fungus Monilinia, which consists mostly of three fungal species: Monilinia laxa, M. fructicola, and M. fructigena. Genomic insights on the eight Monilinia isolates provided a substantial catalogue of genes involved in cellulolysis, pectinolysis, proteolysis, and secondary metabolism. The examination of transcription factor distribution revealed that the transcription factors fungal trans and Zn clus are prevalent in their TFomes. KEGG pathway analysis indicated that Monilinia spp. infection activated multiple pathways involved in carbohydrate catabolism, autophagy, and pentose and glucuronate interconversion for effective colonization. The secretome analysis revealed several putative fungal effectors, and RNA-Seq transcriptome profiling confirmed the expression of many virulence-promoting genes. We also looked at how evolution has influenced the secretome architecture of the fungus and discovered secretome family expansion in Monilinia spp., which might assist in adaptability to both external and internal environments. Furthermore, we discovered that several Monilinia effectors are evolving under positive selection pressure, suggesting that Monilinia spp. may become more fungicide resistant soon. [Display omitted] •Monilinia genomes are enriched with S09X-like peptidases.•Monilinia species contain a highly thermostable Candida antarctica lipase A-like lipases.•Type II PKS genes are absent in all investigated Monilinia isolates.•The Monilinia secretome family is significantly expanding.•Positive selection is driving the evolution of Monilinia effectors.