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.

A novel protein Com1 is required for normal conidium morphology and full virulence in Magnaporthe oryzae.

In Magnaporthe oryzae, pyriform conidia are the primary inoculum and the main source for disease dissemination in the field. In this study, we identified and characterized the COM1 gene that was disrupted in three insertional mutants producing slender conidia. COM1 encodes a putative transcription regulator unique to filamentous ascomycetes. The com1 disruption and deletion mutants had similar defects in conidium morphology and were significantly reduced in virulence on rice and barley seedlings. Microscopic examination revealed that the Deltacom1 mutants were defective in appressorium turgor generation, penetration, and infectious growth. COM1 was expressed constitutively in M. oryzae. The Com1 protein had putative helix-loop-helix structures and three predicted nuclear localization signal sequences. In transformants expressing COM1(335-613)-enhanced green fluorescent protein fusion constructs, fluorescence signals were observed in the nucleus. Our data indicated that the COM1 gene may encode a novel transcription regulator that regulates conidial development and invasive growth in M. oryzae.