Regulating fungal pathogenesis through chromatin modifications
D. COOK (1), M. Seidl (2), M. Kramer (2), B. Thomma (2) (1) Wageningen University, Netherlands; (2) Wageningen University, Netherlands

Plants recognize invading organisms through immune receptors, which must be avoided or subverted to establish a successful symbiosis. A key theme in plant-microbe interactions is that invading organisms utilize effectors, microbially derived molecules, to modulate the plant immune response through varied biochemical processes. Effector expression is tightly regulated and effectors often remain transcriptionally silent outside of specific stages of infection. Despite their importance, mechanistic understanding of how effectors are transcriptionally regulated during growth and infection remains scarce. Recent observations in mainly model fungal systems have begun to link chromatin (the organization of DNA in a cell) to the expression of adaptive genes, but significant questions remain. To address the role of DNA and histone methylation in fungal growth and pathogenesis, we study the soil-borne fungal pathogen Verticillium dahliae. The genome of V. dahliae is predicted to express numerous homologs of chromatin modifying proteins, including three putative DNA methyltransferases. We are using a variety of genetic, proteomic, and computational approaches to characterize the role of DNA and histone modifications in the life history of V. dahliae. We have identified mutants for chromatin modifying proteins that significantly effect fungal growth and plant pathogenesis, including a previously unreported link to DNA methylation. Current data indicate that specific histone modifying proteins negatively regulate effector genes embedded in distinct regions of the genome, and this expression has a strong environmental component. We are studying chromatin dynamics related to gene expression and fungal virulence to elucidate key proteins and pathways regulating these critical proteins.      

Abstract Number: C2-2, P11-388
Session Type: Concurrent