Since the domestication of plants, pathogenic fungi have consistently threatened crop production, evolving genetically to develop increased virulence under various selection pressures. Understanding their evolutionary trends is crucial for predicting and designing control measures against future disease outbreaks. This paper reviews the evolution of fungal pathogens from natural habitats to agricultural settings, focusing on eight significant phytopathogens: Pyricularia oryzae, Botrytis cinerea, Puccinia spp., Fusarium graminearum, F. oxysporum, Blumeria graminis, Zymoseptoria tritici, and Colletotrichum spp. Also, we explore the mechanism used to understand evolutionary trends in these fungi. The studied pathogens have evolved in agroecosystems through either (1) introduction from elsewhere; or (2) local origins involving co-evolution with host plants, host shifts, or genetic variations within existing strains. Genetic variation, generated via sexual recombination and various asexual mechanisms, often drives pathogen evolution. While sexual recombination is rare and mainly occurs at the center of origin of the pathogen, asexual mechanisms such as mutations, parasexual recombination, horizontal gene or chromosome transfer, and chromosomal structural variations are predominant. Farming practices like mono-cropping resistant cultivars and prolonged use of fungicides with the same mode of action can drive the emergence of new pathotypes. Furthermore, host range does not necessarily impact pathogen adaptation and evolution. Although halting pathogen evolution is impractical, its pace can be slowed by managing selective pressures, optimizing farming practices, and enforcing quarantine regulations. The study of pathogen evolution has been transformed by advancements in molecular biology, genomics, and bioinformatics, utilizing methods like next-generation sequencing, comparative genomics, transcriptomics and population genomics. However, continuous research remains essential to monitor how pathogens evolve over time and to develop proactive strategies that mitigate their impact on agriculture.

Cytospora canker (CC) is among the most important diseases in conifer trees (Picea spp., mainly). This disease poses a significant risk factor for forest health, potentially leading to economic losses for wood producers. To provide a genomic basis of the CC pathogenesis, the genomes of two Cytospora species associated with the disease were sequenced and further analyzed within a set of Diaporthales species. The first species was identified as C. piceae. The second was described as C. piceicolasp. nov. based on morphological characteristics and multi-gene phylogenetic analysis. The novel species is sister to other Cytospora species isolated from conifers. Here, we report 39.7 and 43.8 Mb highly contiguous genome assemblies of C. piceae EI-19(A) and C. piceicola EI-20, respectively, obtained using Illumina sequencing technology. Despite notably different genome sizes, these species share the main genome characteristics, such as predicted gene number (10,862 and 10,742) and assembly completeness (97.6% and 98.1%). A wide range of genes encoding carbohydrate-active enzymes, secondary metabolite biosynthesis clusters, and secreted effectors were found. Multiple experimentally validated virulence genes were also identified in the studied species. The defined arsenals of enzymes and effectors generally relate to the hemibiotrophic lifestyle with a capability to switch to biotrophy. The obtained evidence also supports that C. piceae EI-19(A) and C. piceicola EI-20 can cause severe canker disease symptoms in Picea spp. specifically. It was additionally observed that the strains of C. piceae may have different pathogenicity and virulence characteristics based on the analyses of predicted secondary metabolite complements, effectomes, and virulence-related genes. Phylogenomic analysis and timetree estimations indicated that divergence of the studied species may have occurred relatively late, 11-10 million years ago. Compared to other members of Diaporthales, C. piceae EI-19(A) and C. piceicola EI-20 implied a moderate rate of gene contraction, but the latter experienced significant gene loss that can additionally support host specificity attributed to these species. But uncovered gene contraction events may point out potential lifestyle differentiation and host shift of the studied species. It was revealed that EI-19(A) and C. piceicola EI-20 carry distinct secretomes and effectomes among Diaporthales species. This feature can indicate a species lifestyle and pathogenicity potential. These findings highlight potential targets for identification and/or detection of pathogenic Cytospora in conifers. The introduced draft genome sequences of C. piceae and C. piceicola can be employed as tools to understand basic genetics and pathogenicity mechanisms of fungal species causing canker disease in woody plants. The identified pathogenicity and virulence-related genes would serve as potential candidates for host-induced gene silencing aimed at making plant hosts more resistant to pathogenic species. Furthermore, the comparative genomics component of the study will facilitate the functional analysis of the genes of unknown function in all fungal pathogens.

A new ascomycetous species of Parafenestella was isolated from Acer negundo during the survey of diseased trees in Southern Ontario, Canada. The species is morphologically similar to other taxa of Cucurbitariacea (Pleosporales). The new species is different from the extant species in the morphology of ascospores, culture characteristics and molecular data. The novel species is described as Parafenestella ontariensis sp. nov. based on morphological and multi-gene phylogenetic analyses using a combined set of ITS, LSU, tef1 and tub2 loci. Additionally, the genome of P. ontariensis was sequenced and analyzed. The phylogenomic analysis confirmed the close relationship of the species to the fenestelloid clades of Cucurbitariaceae. The comparative genomics analysis revealed that the species lifestyle appears to be multitrophic (necrotrophic or hemi-biotrophic) with a capability to turn pathogenic on a corresponding plant host.

Fusarium is a diverse genus of filamentous fungi that has long been recognized for its importance in plant disease and food security. Beyond its agricultural impact, a growing number of studies now show that Fusarium species can also act as opportunistic pathogens in animals and humans. This review synthesizes current knowledge on Fusarium biology by integrating perspectives from plant pathology, veterinary science, and medical mycology. We examine how shared virulence mechanisms, environmental reservoirs, and genomic plasticity—including accessory chromosomes and horizontal gene transfer—facilitate adaptation across plant, animal, and human hosts. We also consider the role of environmental change in shaping the distribution and pathogenic potential of this genus. By bringing together evidence that is often scattered across disciplines, this review emphasizes the need to move beyond host-specific views and highlights Fusarium as a useful model for understanding fungal adaptability and cross-kingdom pathogenicity within a One Health framework.

Eutypella vitis is reported for the first time on several new host trees viz. Fagus grandifolia, Fraxinus pennsylvanica and Syringa reticulata with associated branch dieback symptoms in the Niagara Region of Southern Ontario, Canada. Morphological characteristics and phylogenetic analyses of ITS sequence data confirmed the species identification. Eutypella vitis is known as a woody plant pathogen causing dieback of grapevines and other economically important fruit trees widely cultivated in Ontario. The fungus ability to infect several alternate new hosts can promote its faster and wider spread across vineyards and consequently increase a dieback hazard to viticulture in Canada.