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ARS Home » Southeast Area » Stuttgart, Arkansas » Dale Bumpers National Rice Research Center » Research » Publications at this Location » Publication #231406
Title: Understanding the molecular mechanisms of rice blast resistance using rice mutants

Author
item Jia, Yulin

Submitted to: Symposium Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 8/15/2008
Publication Date: 10/1/2009
Citation: Jia, Y. 2009. Understanding the molecular mechanisms of rice blast resistance using rice mutants. Shu, Q.Y., editor, Induced Plant Mutations in the Genomics Era. Food and Agriculture Organization of the United Nations, Rome. p. 375-378.

Interpretive Summary:

Technical Abstract: Induced mutation can be useful for studying resistance gene controlled plant immunity. Resulting knowledge should benefit the development of strategies for crop protection. The Pi-ta gene in rice has been effectively deployed for preventing rice blast disease-the most devastating disease of rice worldwide. Pi-ta was introgressed into diverse cultivars in the US and Japan from landrace indica varieties, Tetep and Taducan, respectively. Pi-ta was predicted to be a cytoplasmic receptor that directly binds to the elicitor produced by the pathogen avirulence gene AVR-Pita for initiating resistance [1, 2]. Alanine located at position 918 of the Pi-ta protein in the region predicted to be involved in ligand binding has been shown to determine the binding specificity. Here I report the identification of a second gene, Ptr(t), required by Pi-ta for resistance. Katy, a tropical japonica cultivar from the US, expressing resistance condtioned by Pi-ta and Pi-ks to the common races of M. oryzae, IB1, IB45, IB49, IB54, IC17, IH1, IE1, and IG1 was treated with fast neutrons. Five susceptible M2 mutants were identified by screening seedlings derived from 10,000 M1 plants. Among them a stable mutant M2354 was found susceptible to IB1, IB45, IB49, IC17, IH1, IE1, and IG1 conditioned by Pi-ta and resistant to IB54 conditioned by Pi-ks. The DNA sequences of the Pi-ta gene in M2354 was found unchanged based on PCR-sequencing. Expression of Pi-ta in M2354 was also found identical to that of the mother parent examined by qRT-PCR and real time RT-PCR. Thus, mutations in M2354 likely occurred at a new locus specific to Pi-ta-mediated resistance. Genetic analysis and genotyping the Pi-taptr(t), Pi-taPtr(t), pi-taptr(t) homozygotes revealed that Pi-ta and Ptr(t) co-segregate and are located within a 9 megabase genomic region on chromosome 12 [3]. These findings provide a starting point to isolate Ptr(t) and dissect the Pi-ta mediated signaling pathways leading to resistance.