A mitogen-activated protein kinase gene (VmPmk1) regulates virulence and cell wall degrading enzyme expression in Valsa mali.

Mitogen-activated protein kinases (MAPKs) play critical roles in the regulation of different developmental processes and hydrolytic enzyme production in many fungal plant pathogens. In this study, an FUS3/KSS1-related MAPK gene, VmPmk1, was identified and characterized in Valsa mali, which causes a highly destructive canker disease on apple. VmPmk1 deletion mutant showed a significant reduction in growth rate in vitro, and could not produce pycnidium, indicating that the MAPK gene is important for growth and asexual development. Also, VmPmk1 played a significant role in response to oxidative stress and in the maintenance of cell wall integrity. More importantly, when deletion mutant was inoculated onto detached apple leaves and twigs, an obvious decrease in lesion size was observed. Furthermore, expression of many cell wall degrading enzyme (CWDE) genes declined in the VmPmk1 deletion mutant during infection. VmPmk1 deletion mutant also showed a significant reduction in activities of CWDEs in both induced media and infection process. Finally, the determination of immunogold labeling of pectin demonstrated that the capacity of degradation pectin was attenuated due to the deletion of VmPmk1. These results indicated that VmPmk1 plays important roles in growth, asexual development, response to oxidative stress, and maintenance of cell wall integrity. More importantly, VmPmk1 is involved in pathogenicity of V. mali mainly by regulating CWDE genes expression.

Genome sequence of Valsa canker pathogens uncovers a potential adaptation of colonization of woody bark.

Canker 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.