RESUMO
The emergence of new fungal pathogens threatens sustainable crop production worldwide. One mechanism by which new pathogens may arise is hybridization. To investigate hybridization, the related smut fungi, Ustilago maydis and Sporisorium reilianum, were selected because they both infect Zea mays, can hybridize, and tools are available for their analysis. The hybrid dikaryons of these fungi grew as filaments on plates but their colonization and virulence in Z. mays were reduced compared to the parental dikaryons. The anthocyanin induction caused by the hybrid dikaryon infections was distinct, suggesting its interaction with the host was different from that of the parental dikaryons. Selected virulence genes previously characterized in U. maydis and their predicted S. reilianum orthologs had altered transcript levels during hybrid infection of Z. mays. The downregulated U. maydis effectors, tin2, pit2, and cce1, and transcription factors, rbf1, hdp2, and nlt1, were constitutively expressed in the hybrid. Little impact was observed with increased effector expression; however, increased expression of rbf1 and hdp2, which regulate early pathogenic development by U. maydis, increased the hybrid's capacity to induce symptoms including the rare induction of small leaf tumors. These results establish a base for investigating molecular aspects of smut fungal hybrid pathogen emergence.
RESUMO
Biotrophic basidiomycete plant pathogens cause billions of dollars in losses to cereal crops annually. The model for this group of fungi is the corn smut pathogen Ustilago maydis. Annotation of its genome identified antisense RNAs (asRNAs) complementary to over half of the coded mRNAs, some of which are present at high levels in teliospores but detected at very low levels or not at all in other cell types, suggesting they have a function in the teliospore or during teliospore formation. Expression of three such asRNAs (as-UMAG_02150, ncRNA1, and as-UMAG_02151) is controlled by two adjacent genomic regions. Deletion of these regions increased transcript levels of all three asRNAs and attenuated pathogenesis. This study investigated the reason for this marked reduction in pathogenesis by: (1) using deletion analyses to assess the involvement of genes, complementary to the asRNAs, in pathogenesis; (2) determining that one of the linked genes encodes a putative xylitol dehydrogenase; and (3) identifying and functionally characterizing asRNAs that could influence expression of protein-coding genes. The results presented suggest that the influence of the asRNAs on pathogenesis occurs through their action at unlinked loci.
