A review in Plant Cell from Darren Soanes and colleagues summarizes some of the major findings about evolution of phytopathogenic fungi gleaned from genome sequencing highlighting 12 fungi and 2 oomycetes. By mapping evolution of genes identified as virulence factors as well as genes that appear to have similar patterns of diversification, we can hope to derive some principals about how phytopathogenic fungi have evolved from saprophyte ancestors.
They infer from phylogenies we’ve published (Fitzpatrick et al, James et al) that plant pathogenic capabilities have arisen at least 5 times in the fungi and at least 7 times in the eukaryotes. In addition they use data on gene duplication and loss in the ascomycete fungi (Wapinski et al) to infer there large numbers of losses and gains of genes have occurred in fungal lineages.
The findings of large numbers of GPCR in many filamentous ascomycete fungi including as many as 61 in the Magnaporthe grisea (Dean et al) and 84 in the Fusarium graminearum (Cuomo et al) genomes also suggest phytopathogenic fungi have an expanded repertoire for detecting and responding to biotic and abiotic cues. What is still missing is detailed analyses pinpointing the exact timing of this family diversification, and whether it is actually a significant expansion or can be equally explained by drift. Analysis of the gene trees for these families can better identify the young and old copies of the genes to see if there are a class that may represent recent adaptation to a plant host.
The authors go on to talk about the numbers of secreted proteins in these genomes. It seems to me like we have yet to connect the predictions from the genome to actual observed molecules beyond some general trends. However, they highlight some of the interesting examples such as the the large fraction of secreted proteins in Ustilago maydis arranged in 12 clusters (Kamper et al) but most with no known function. Analyses of effector proteins in Oomycetes found large class of these in both the sudden oak death (P. ramorum) and soybean rust (P. sojae) but little overlap in these effectors genes with genes found in fungi.
The authors also discuss secondary metabolites enzymes (PKS, NRPS, P450) and the broad range of toxin and other metabolites biosynthesis capabilities in filamentous fungi. Fungi use these different metabolites to manipulate the plant host: from calcium signaling to growth regulators, to various biotoxins. The expansion and diversification of these happened at different points in fungal evolution, although I am not convinced that the initial expansion directly lead to pathogenic capabilities, but rather was part of expanding saprobe lifestyles to try and establish territory.
I’m excited about the syntheses we are able to achieve now with available functional and evolutionary data. With our ongoing work looking at the genomes of early branches of the fungal tree including the Chytrids we should have additional resolution to map numbers and types changes in gene families that have lead to lifestyle changes for saprobes, phytopathogens, animal pathogens, and rise of multicellular and developmental lifestages.
Soanes, D.M., Richards, T.A., Talbot, N.J. (2007). Insights from Sequencing Fungal and Oomycete Genomes: What Can We Learn about Plant Disease and the Evolution of Pathogenicity?. THE PLANT CELL ONLINE, 19(11), 3318-3326. DOI: 10.1105/tpc.107.056663