SummaryCanker caused by ascomycetous Valsa species are among the most destructive diseases of woody plants worldwide. These pathogens are distinct from other pathogens because they only effectively attack tree bark in the field. To unravel the potential adaptation mechanism of bark colonization, we examined the genomes of Valsa mali and Valsa pyri that preferentially infect apple and pear, respectively.We reported the 44.7 and 35.7 Mb genomes of V. mali and V. pyri, respectively. We also identified the potential genomic determinants of wood colonization by comparing them with related cereal pathogens.Both genomes encode a plethora of pathogenicity-related genes involved in plant cell wall degradation and secondary metabolite biosynthesis. In order to adapt to the nutrient limitation and low pH environment in bark, they seem to employ membrane transporters associated with nitrogen uptake and secrete proteases predominantly with acidic pH optima. Remarkably, both Valsa genomes are especially suited for pectin decomposition, but are limited in lignocellulose and cutin degradation. Besides many similarities, the two genomes show distinct variations in many secondary metabolism gene clusters.Our results show a potential adaptation of Valsa canker pathogens to colonize woody bark. Secondary metabolism gene clusters are probably responsible for this host specificity.
Summary Pathogen‐associated molecular patterns (PAMPs) are conserved molecules that are crucial for normal life cycle of microorganisms. However, the diversity of microbial PAMPs is little known. During screening of cell‐death‐inducing factors from the necrotrophic fungus Valsa mali, we identified a novel PAMP VmE02 that is widely spread in oomycetes and fungi. Agrobacterium tumefaciens‐mediated transient expression or infiltration of recombinant protein produced by Escherichia coli was performed to assay elicitor activity of the proteins tested. Virus‐induced gene silencing in Nicotiana benthamiana was used to determine the components involved in VmE02‐triggered cell death. The role of VmE02 in virulence and conidiation of V. mali were characterized by gene deletion and complementation. We found that VmE02, together with some of its homologues from both oomycete and fungal species, exhibited cell‐death‐inducing activity in N. benthamiana. VmE02‐triggered cell death was shown to be dependent on BRI1‐ASSOCIATED KINASE‐1, SUPPRESSOR OF BIR1‐1, HSP90 and SGT1 in N. benthamiana. Deletion of VmE02 in V. mali greatly attenuated pathogen conidiation but not virulence, and treatment of N. benthamiana with VmE02 enhances plant resistance to Sclerotinia sclerotiorum and Phytophthora capsici. We conclude that VmE02 is a novel cross‐kingdom PAMP produced by several fungi and oomycetes.
Velvet protein family members are important fungal-specific regulators which are involved in conidial development, secondary metabolism and virulence. To gain a broader insight into the physiological functions of the velvet protein family of Valsa mali, which causes a highly destructive canker disease on apple, we conducted a functional analysis of two velvet protein family members (VmVeA and VmVelB) via a gene replacement strategy. Deletion mutants of VmVeA and VmVelB showed increased melanin production, conidiation and sensitivity to abiotic stresses, but exhibited reduced virulence on detached apple leaves and twigs. Further studies demonstrated that the regulation of conidiation by VmVeA and VmVelB was positively correlated with the melanin synthesis transcription factor VmCmr1. More importantly, transcript levels of pectinase genes were shown to be decreased in deletion mutants compared with those of the wild-type during infection. However, the expression of other cell wall-degrading enzyme genes, including cellulase, hemi-cellulase and ligninase genes, was not affected in the deletion mutants. Furthermore, the determination of pectinase activity and immunogold labelling of pectin demonstrated that the capacity for pectin degradation was attenuated as a result of deletions of VmVeA and VmVelB. Finally, the interaction of VmVeA with VmVelB was identified through co-immunoprecipitation assays. VmVeA and VmVelB play critical roles in conidiation and virulence, probably via the regulation of the melanin synthesis transcription factor VmCmr1 and their effect on pectinase gene expression in V. mali, respectively.
The identification of effectors from pathogenic microbes is one of the most important subjects for elucidating infection mechanisms. Wheat blue dwarf (WBD) phytoplasma causes dwarfism, witches' broom, and yellow leaf tips in wheat plants, resulting in severe yield loss in northwestern China. In this study, 37 candidate effector proteins were transiently expressed in Nicotiana benthamiana. Plants expressing the SAP11-like protein SWP1 exhibited typical witches' broom. Interestingly, another protein, SWP11, induced both cell death and defence responses, including H 2 O 2 accumulation and callose deposition. Analysis by qRT-PCR was used to show that a marker gene of the hypersensitive response, HIN1, and three pathogenesis-related genes, PR1, PR2 and PR3, were significantly up-regulated in leaves of N. benthamiana expressing SWP11. In addition, SWP12 and SWP21 (TENGU-like) were shown to suppress SWP11-, BAX-, and/or INF1-induced cell death. These results indicated that SWP21 has a distinct role in virulence compared with TENGU and that WBD phytoplasma possesses effectors that target plant proliferation and defence responses. The ability of these effectors to trigger or suppress plant immunity provides new insights into the phytoplasma-plant interaction.
Apple Valsa canker is a destructive disease caused by the ascomycete Valsa mali and poses a serious threat to apple production. Toxins synthesized by secondary metabolite biosynthetic gene clusters (SMBGCs) have been proven to be crucial for pathogen virulence. A previous study showed that V. mali genome contains remarkably expanded SMBGCs and some of their genes were significantly upregulated during infection. In this study, we focus on LaeA, a known regulator of secondary metabolism, for its role in SMBGC regulation, toxin production, and virulence of V. mali. Deletion of VmLaeA led to greatly reduced virulence with lesion length reduced by 48% on apple twigs. Toxicity tests proved that toxicity of secondary metabolites (SMs) produced by VmLaeA deletion mutant (VmlaeA) was markedly decreased in comparison with wildtype (WT). Transcriptomic and proteomic analyses of WT and VmlaeA indicated that a portion of transporters and about half (31/60) SMBGCs are regulated by VmLaeA. Function analysis of eight gene clusters including PKS7, PKS11, NRPS14, PKS16, PKS23, PKS31, NRPS/PKS33, and PKS39 that were differentially expressed at both transcriptional and translational levels showed that four of them (i.e., PKS11, PKS16, PKS23, and PKS31) were involved in pigment production and NRPS14 contributed to virulence. Our findings will provide new insights and gene resources for understanding the role of pathogenicity-related toxins in V. mali.
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