Abstract

Pyrenophora tritici-repentis (Ptr), causal agent of tan spot of wheat, is a necrotrophic fungus that presents an increasing threat to wheat production due to its rapid, global expansion. Despite its homothallic nature, Ptr populations have high genetic diversity, which positively impacts host range and virulence. Pathogenicity by Ptr is attributable to the production of host-selective toxins (HSTs) and follows an inverse gene-for-gene mechanism, in which HSTs are recognized by unique single dominant genes that confer both toxin-sensitivity and disease susceptibility. Studies addressing the mechanism of action of Ptr HSTs have unveiled both commonalities and complexities of the host response to these toxins. Resistance-like host responses triggered by the HSTs support the emerging hypothesis that necrotrophic pathogens exploit the host defense response as a mechanism to induce host cell death and ensure colonization. Recent advances in sequencing technology have facilitated the comparison of the genetic makeup of pathogenic and nonpathogenic isolates of Ptr. Such comparisons are providing insights into the genetic diversity of the pathogen and the mechanisms that dictate the increase in virulence and incidence of this important pathogen. Comparative genome analysis has also provided evidence that transposable elements (TEs) play a crucial role in genome re-arrangement and expansion, which contributes to the genomic flexibility to create and diversify effectors.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call