Submitted to: Rice Technical Working Group Meeting Proceedings
Publication Type: Proceedings
Publication Acceptance Date: January 15, 2008
Publication Date: March 1, 2008
Citation: Jia, Y. 2008. Mechanisms of Rice Blast Resistance and Its Implication for Breeding for Improved Resistance. In: Proceedings of the 32nd Rice Technical Working Group Meetings, February 18-21, 2008, San Diego, CA. 2008. CDROM. Technical Abstract: A major Pyricularia (Pi) resistance (R) gene to the blast pathogen M. oryzae prevents only isolates of M. oryzae that contain the corresponding avirulence (AVR) genes. The AVR genes in M. oryzae are presumably meant to promote diseases and are often evolved for the adaptation and fitness of the pathogen. Despite over 40 major Pi genes that have been described, and seven of which have been isolated in rice germplasm worldwide, the R genes in rice are outnumbered by the AVR genes in the pathogen. In addition, most isolated blast R genes were predicted to be cytoplasmic proteins with NBS-LRR domain that are the most pre-dominant type of R genes in the plant kingdom. An outstanding question arises: How are these conserved blast R genes in rice able to cope with the AVR genes in the pathogen? To address this question, a detailed analysis of structural and functional properties of a blast R gene Pi-ta and the corresponding AVR gene AVR-Pita has been undertaken in the USDA-ARS Dale Bumpers National Rice Research Center. Pi-ta is a single gene located at 10.6 megabase (MB) near the centromere (12 MB) of rice chromosome 12. Pi-ta in different genetic backgrounds has been shown to vary in resistance effectiveness. Mechanisms of alternative splicing in Pi-ta resistance are being investigated to determine if expression of these different transcripts of Pi-ta has any functional correlations to the resistance (Costanzo and Jia, poster in this meeting). Results of genetic studies suggest Pi-ta requires a new locus [Ptr(t)]for recognizing the pathogen signals. In addition, another R gene Pi-ta2 was also mapped near Pi-ta, and both Pi-ta and Pi-ta2 required the same locus [Ptr(t)] to be functional. All of them are mapped at the Pi-ta region. These findings suggest that R genes and their required components are clustered in a small genetic region that is one of the most effective systems to fight against the pathogen. AVR-Pita encoding a putative metalloprotease with a protease motif, located near the telomeres of chromosome 3 of some isolates, is induced during the invasive growth of the pathogen. A protease with intact motif in M. oryzae is essential for its function in pathogenesis, however, this may become an advantage for Pi-ta to recognize AVR-Pita in triggering sophisticated multifaceted defense responses. In fact, amino acid substitutions of AVR-Pita are often observed in other regions of the protein, and these alterations are presumed advantageous for pathogenesis, and for other essential needs for the survival of the pathogen. A compressive study utilizing classical techniques of biochemistry and molecular biology is being undertaken to unravel the molecular interactions of Pi-ta with AVR-Pita. New knowledge learned from this system is being used to design the genetic strategies to prevent blast disease. Progress in this endeavor will be presented.