Race structure of in the Kansas wheat pathogen population.

Plant Dis

Kansas State University, Plant Pathology, 4024 Throckmorton PSC, Manhattan, Kansas, United States, 66506.

Published: December 2024

AI Article Synopsis

  • Tan spot, a wheat disease caused by the pathogen Pyrenophora tritici-repentis, involves three necrotrophic effectors (Ptr ToxA, Ptr ToxB, and Ptr ToxC), and its variations are sorted into a race system based on their genetic combinations.
  • A survey in Kansas identified 63 isolates of Ptr, revealing that race 1, which includes the harmful Ptr ToxA, is the most prevalent, along with the existence of races 2, 3, and 4.
  • These findings suggest that wheat breeding efforts in Kansas should aim to reduce the susceptibility gene Tsn1 to enhance resistance against the pathogen, providing valuable insights for breeders and path

Article Abstract

Tan spot, caused by Pyrenophora tritici-repentis (Ptr) carries any of at least three identified necrotrophic effectors (NE) as part of its host invasion repertoire (Ptr ToxA, Ptr ToxB, and Ptr ToxC). The 8 possible combinations of these genes, or their absence, are described using a race system. These races characterize the disease phenotype observed on a wheat differential set. The primary NE, Ptr ToxA, enables pathogenesis through an interaction with the wheat susceptibility gene, Tsn1. This study aimed to determine the race structure of the Ptr population in Kansas. To complete this objective, a survey was conducted to collect isolates of the pathogen from the Kansas wheat production region. In addition, 16 historic isolates were also included. The isolates were screened against the wheat differential set, and molecularly characterized for presence of the genes ToxA, and ToxB, and a non-functioning ToxB haplotype called toxb. The survey identified 63 Ptr isolates. Our results revealed the predominance of race 1, which contains ToxA and ToxC. However, we also identified isolates of race 2, 3, and 4. The results of molecular assays matched the screening results for Ptr ToxA and Ptr ToxB in most cases. Some isolates caused atypical symptoms which did not match the current race structure. The prevalence of race 1 Ptr in the Kansas population suggests that breeding for resistance in Kansas should focus on selecting against Tsn1 which encodes susceptibility to Ptr ToxA. This research provides critical insights that will inform breeders and pathologists for improved control of Ptr.

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Source
http://dx.doi.org/10.1094/PDIS-11-24-2441-REDOI Listing

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