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ARS Home » Southeast Area » Stuttgart, Arkansas » Dale Bumpers National Rice Research Center » Research » Publications at this Location » Publication #159205
Title: HOW DOES THE RICE BLAST PATHOGEN DEFEAT A RESISTANCE GENE?

Author
item CORRELL, JAMES - DEPT PLANT PATH, UAF
item Jia, Yulin
item BOZA, E - DEPT PLANT PATH, UAV
item SINGH, PRATIBHA - UA RREC
item LEE, FLEET - UA RREC

Submitted to: Rice Technical Working Group Meeting Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 2/29/2004
Publication Date: 2/1/2005
Citation: Correll, J.C., Jia, Y., Boza, E.G., Singh, P., Lee, F. 2005. How does the rice blast pathogen defeat a resistance gene? Rice Technical Working Group Meeting Proceedings. Abstract p. 104.

Interpretive Summary:

Technical Abstract: In practice, the term "durable resistance" is typically applied to a resistance that remains effective over a wide area for a long period of time in the presence of disease and favorable environmental conditions for disease development. In Arkansas, the Pi-ta resistance gene can be considered a durable resistance gene. The cultivar Katy, which contains Pi-ta, was first released in the early 1980's as a blast-resistant cultivar. Although isolates have been identified which can overcome the Pi-ta resistance gene in Katy and other cultivars, there have not been any documented epidemics where a cultivar with Pi-ta has suffered a yield-reducing epidemic in a commercial rice field. Therefore, Pi-ta still remains effective in Arkansas. The objective of this study was to examine the mechanism by which isolates of the rice blast pathogen overcome the Pi-ta resistance gene. We have recovered field isolates and greenhouse-generated "race shift" mutants that can overcome the Pi-ta resistance gene under greenhouse screening conditions. The field isolates with this phenotype were recovered from different areas of the state and all belong to a single MGR586 DNA fingerprint group (group B). In addition, the frequency of the race shift mutants with this phenotype recovered in greenhouse studies was much higher in the group B isolates. In an effort to determine how isolates overcome Pi-ta resistance, we have focused on how the avirulence gene AVR-Pita is altered in both field and greenhouse isolates. Evidence thus far indicates that field isolates virulent on lines with the Pi-ta resistance gene are lacking AVR-Pita. Also, although AVR-Pita can be detected in avirulent field isolates, the race shift mutants virulent on lines with Pi-ta recovered from these parental strains lack the AVR-Pita gene. Thus, PCR amplifications and southern blotting indicates that all or a significant portion of the AVR-Pita gene is deleted, or becomes undetectable, in these isolates. There are several hypotheses that could explain the durability of Pi-ta in Arkansas. One hypothesis is that environmental conditions are variable and not necessarily conducive for disease development each year and Pi-ta has not be adequately challenged; a second hypothesis is that isolates which lose AVR-Pita and become virulent on lines with Pi-ta also have reduced fitness and do not become established in the population.