Comparative genomics of a plant-pathogenic fungus, pyrenophora tritici-repentis, reveals transduplication and the impact of repeat elements on pathogenicity and population divergence

Pyrenophora tritici-repentis is a necrotrophic fungus causal to the disease tan spot of wheat, whose contribution to crop loss has increased significantly during the last few decades. Pathogenicity by this fungus is attributed to the production of host-selective toxins (HST), which are recognized by their host in a genotype-specific manner. To better understand the mechanisms that have led to the increase in disease incidence related to this pathogen, we sequenced the genomes of three P. tritici-repentis isolates. A pathogenic isolate that produces two known HSTs was used to assemble a reference nuclear genome of approximately 40 Mb composed of 11 chromosomes that encode 12,141 predicted genes. Comparison of the reference genome with those of a pathogenic isolate that produces a third HST, and a nonpathogenic isolate, showed the nonpathogen genome to be more diverged than those of the two pathogens. Examination of gene-coding regions has provided candidate pathogen-specific proteins and revealed gene families that may play a role in a necrotrophic lifestyle. Analysis of transposable elements suggests that their presence in the genome of pathogenic isolates contributes to the creation of novel genes, effector diversification, possible horizontal gene transfer events, identified copy number variation, and the first example of transduplication by DNA transposable elements in fungi.Overall, comparative analysis of these genomes provides evidence that pathogenicity in this species arose through an influx of transposable elements, which created a genetically flexible landscape that can easily respond to environmental changes

Induction of defense responses in tobacco by the protein Nep1 from Fusarium oxysporum

Fusarium oxysporum produces a 24-kDa protein, Nep1, which induces necrosis and ethylene production in leaves of many dicot plant species. Detached Nicotiana tabacum L. cv. Xanthi leaves respond with concentration-dependent necrosis after infiltration with Nep1 or when Nep1 is taken up by the vascular tissue. This response follows the induction of ethylene biosynthesis and accumulation of ACC synthase and ACC oxidase transcripts. Pretreating the leaves with 100 µl/l ethylene prior to elicitation enhanced Nep1-induced ethylene production. Nep1 (208 nM) causes extensive necrosis of mature tobacco leaf tissue when applied to Xanthi tobacco as a foliar spray (129 ml/m2). Tobacco cell cultures respond to Nep1 by alkalization of the culture media, the accumulation of potassium in the media, oxygen uptake, induction of active oxygen species, and eventual cell death. The response of cultured tobacco cells to Nep1 is time- and concentration-dependent. Cell death was the same at 300 min for 5 ng/ml and higher concentrations, while 0.5 ng/ml had no effect on cell death. In the case of O2 uptake, cells responded to 0.5 ng/ml within minutes of treatment, but at a rate lower than 5 ng/ml. The lower concentration of Nep1 did not induce an increase in pH, K+ efflux, or increasing H2O2 accumulation in the culture media