Divergent and Convergent Evolution of Fungal Pathogenicity

Abstract

Fungal pathogens of plants and animals have multifarious effects; they cause devastating damages to agricultures, lead to life-threatening diseases in humans, or induce beneficial effects by reducing insect pest populations. Many virulence factors have been determined in different fungal pathogens; however, the molecular determinants contributing to fungal host selection and adaptation are largely unknown. In this study, we sequenced the genomes of seven ascomycete insect pathogens and performed the genome-wide analyses of 33 species of filamentous ascomycete pathogenic fungi that infect insects (12 species), plants (12), and humans (9). Our results revealed that the genomes of plant pathogens encode more proteins and protein families than the insect and human pathogens. Unexpectedly, more common orthologous protein groups are shared between the insect and plant pathogens than between the two animal group pathogens. We also found that the pathogenicity of host-adapted fungi evolved multiple times, and that both divergent and convergent evolutions occurred during pathogen–host cospeciation thus resulting in protein families with similar features in each fungal group. However, the role of phylogenetic relatedness on the evolution of protein families and therefore pathotype formation could not be ruled out due to the effect of common ancestry. The evolutionary correlation analyses led to the identification of different protein families that correlated with alternate pathotypes. Particularly, the effector-like proteins identified in plant and animal pathogens were strongly linked to fungal host adaptation, suggesting the existence of similar gene-for-gene relationships in fungus–animal interactions that has not been established before. These results well advance our understanding of the evolution of fungal pathogenicity and the factors that contribute to fungal pathotype formation.

Metabolic Conservation and Diversification of Metarhizium Species Correlate with Fungal Host-Specificity

“…On the other hand, this observation also raises the question whether the gene cluster was lost in specialists or acquired in non-specialist species. Metarhizium species evolved after the divergence of the ascomycete plant pathogenic fungi (Shang et al, 2016; Wang et al, 2016), and the specialist species evolved first (Hu et al, 2014). To adapt to diverse insect hosts, it is possible that the non-specialists acquired the toxin-producing gene cluster during their speciation processes.…”

PHI-base: a new interface and further additions for the multi-species pathogen–host interactions database

“…All articles are listed in the ‘about’ section of the website to provide database use examples. New uses for PHI-base data include (i) comparative analysis of the genomes of fungi that infect insects in natural ecosystems and alter insect behavior to favor fungal spore dispersal (18,19), (ii) characterization of the potential virulence genes within the genomes of eight dematiaceous fungal species which infect humans in tropical regions (20) or facilitate ascomycete fungal endoparasitism of nematodes (21), (iii) exploration of divergent and convergent evolution of fungal pathogenicity in insect, plant and human hosts (22) and (iv) studying the rate of horizontal gene transfer events from pathogenic bacteria to plant pathogenic fungi (23). …”

A transcription factor, MrMsn2, in the dimorphic fungus Metarhizium rileyi is essential for dimorphism transition, aggravated pigmentation, conidiation and microsclerotia formation

“…In addition, the amino acid sequence of MrMsn2 showed similarities (79–81% identity) to a cutinase G‐box binding protein of Metarhizium spp. (Hu et al ., 2014; Shang et al ., 2016) and a zinc finger protein (66% identity) of Tolypocladium ophiglossoides (Quandt et al ., 2015). …”

“…The resultant plasmid was named pPZP‐Hph‐ msn2 . For the mutant complementation strains, the open reading frame (ORF) of MrMsn2 with the promoter and terminator regions, was amplified based on the subsequently public annotated of the M. rileyi genome (Shang et al ., 2016) using the primers Ms‐HF/Ms‐HR (Table S1). PCR products were digested by restriction endonucleases and ligated into the sulfonylurea resistance vector pPZP‐Sur‐Knock to generate the plasmid, pPZP‐Sur‐ msn2 .…”

“…We also found that M. rileyi MrMsn2 was predicted to function downstream of the HOG pathway and was upregulated during MS formation in comparative transcriptome analysis (Song et al ., 2013). Furthermore, a bioinformatics analysis found no Msn4 orthologues in any public genome databases of M. rileyi (Song et al ., 2013; Shang et al ., 2016). These results imply a possible involvement of MrMsn2 in the regulation of MS development.…”