W330 Sequencing and resequencing the necrotrophic Dothideomycete, Pyrenophora tritici-repentis, provides insights into the biology of an increasingly significant wheat pathogen

Date: Monday, January 16, 2012
Time: 2:05 PM
Room: Sunset
Viola Manning , Oregon State University, Corvallis, OR
Li-Jun Ma , University of Massachusetts, Amherst, MA
Igor V. Grigoriev , US DOE Joint Genome Institute, Walnut Creek, CA
Larry J. Wilhelm , Oregon State University, Corvallis, OR
Braham Dhillon , University of British Columbia, Vancouver, Canada
Iovanna Pandelova , Oregon State University, Corvallis, OR
Wade H. Holman , Oregon State University, Corvallis, OR
Lynda M. Ciuffetti , Oregon State University, Corvallis, OR
Pyrenophora tritici-repentis (Ptr) is the fungal pathogen causal to the disease tan spot of wheat.  Host-selective toxins (HSTs), which define the race structure of Ptr, are major virulence factors in this interaction. Although there is a high degree of genetic variability in Ptr populations that does not correlate with race structure, non-pathogenic isolates are often more similar to each other than to pathogenic isolates.  To better understand the mechanisms of pathogenesis of Ptr, and the differences between pathogenic and non-pathogenic isolates, we obtained a reference genome sequence of a pathogenic race 1 isolate (BFP) that produces the HSTs Ptr ToxA & C and we resequenced two additional isolates - a pathogenic race 5 that produces Ptr ToxB and a non-pathogenic race 4 (SD20).  In addition, we sequenced transcripts from BFP, SD20 and the pathogenic isolate, SO3, which produces an uncharacterized HST. An optical map of the reference genome consists of 11 linkage groups and estimated genome size of ~40 Mb.  Mapping of resequenced isolate sequences and ESTs onto the reference indicated that pathogens are more similar to each other than to the non-pathogen. More repeat families, especially DNA transposons, are shared between the pathogen genomes. Approximately 93% of predicted loci and 96% of secreted proteins are shared by all sequenced isolates.  Discontinuous secondary metabolite clusters may point to uncharacterized pathogenicity factors.  Importantly, duplication of partial or entire genes and larger genome fragments are easily identifiable in the Ptr genome and are likely to represent an important mechanism for effector diversification.