Scientists reveal novel strategy of preventing chitin-triggered host immunity by soil-borne fungal pathogens

The main component in the fungal cell wall, chitin, is required to maintain the structure of the fungal cell, but it is also a strong elicitor of plant resistance which will hinder the progression of the pathogen. Chitin oligomers act as microbe-associated molecular patterns recognized by plant transmembrane LysM receptor kinases/proteins and initiate chitin-triggered host immunity. The capacity of the fungus to escape from recognition determines the success of the fungal pathogen to colonize the plant. Several leaf-infecting fungal pathogens deliver LysM effectors to bind chitin oligomers perturbing host chitin perception. However, LysM effectors of soil-borne fungal pathogens do not perturb host chitin perception. It remains elusive how soil-borne fungal pathogens overcome chitin-triggered host immune response.

Recently, the group of Dr. Guo Hui-Shan in the State Key Laboratory of Plant Genomics, Institute of Microbiology (IM), Chinese Academy of Sciences, identify a secretory polysaccharide deacetylase, VdPDA1, from a soil-borne pathogenic fungus, Verticillium dahliae, the most notorious plant pathogen of the Verticillium genus, that facilitates infection through direct deacetylation of chitin oligomers, leading to suppression of plant LysM chitin receptor perception and dimerization. Moreover, a phylogenetics analysis of 5714 fungal proteins with conserved polysaccharide deacetylase domains showed that the VdPDA1-containing subtree includes a large number of proteins with conserved polysaccharide deacetylase domains from the Verticillium genus and the Fusarium genus, another group of characterized soil-borne fungal pathogens. Further analysis showed that a Fusarium PDA also possesses deacetylase activity and is required for virulence during plant infection, suggesting that soil-borne fungal pathogens have adopted chitin deacetylation as a major virulence strategy.