Rice Genetics IV - IRRI books - International Rice Research Institute

analysis suggests that the mutation in GR-740-12-8 is dominant. Another gammaray-inducedmutant, GR-978-18-18, shows strong resistance to 10 races of Xoo fromthe Philippines and to two isolates of the blast pathogen. This mutant is slightly shorterthan the wild-type IR64. Another mutant, GR-282-12-15, showed a gain in resistanceto a single isolate of Xoo and two blast isolates. Segregation patterns in the M 3 generationsuggest that both mutations in GR-978-18-18 and in GR-282-12-15 are recessive.Overall, a majority of these gain-in-resistance mutants are morphologically abnormal,ranging from semidwarf to severe stunting. In Arabidopsis, some gain-inresistancemutants were also morphologically abnormal (Clough et al 2000). As ofnow, we have not identified mutants showing susceptibility to multiple pathogens,indicating a need to expand the screening to detect these presumably rare mutations.The most common class of disease-response mutants is those with lesion mimics.Yin et al (2000) demonstrated that some but not all lesion mimic mutants (in anothergenetic background of indica rice IR68) exhibit enhanced resistance to blast and bacterialblight. To further delineate the pathways involved in disease and defense responses,we selected 21 lesion mimic mutants from the IR64 mutant collection. Wefound that these mutants showed a varying degree of enhanced resistance to differentbacterial blight strains and that resistance was not race-specific. Two mutants, D6-1851 and D6-242, with reduced resistance to Xoo and M. grisea were monitored forexpression of a pathogenesis-related (PR) protein gene PBZ1 (Fig. 2). In the wildtypeand single mutants, the expression of PBZ1 was strongest in the second youngestleaf (L2) but decreased in the older leaves (L3 and L4). In the double mutant, whichshowed enhanced resistance, high expression of PBZ1 was maintained in the olderleaves.Double mutants have been created by crossing independently inherited lesionmimic mutants to evaluate the epistatic relationships among these mutations. Defenseresponse (DR) genes PR-1, peroxidase 22.3 (POX22.3), and peroxidase POC1(POC1) were used to probe mRNA from four leaf stages of the single and doublemutants derived from D6-1851 × D6-242. POX22.3 expression was high in youngleaves and diminished as lesions developed. PR-1 and POC1 expression was enhancedrelative to that observed in IR64 in the second and third leaves. In general, DR geneexpression was positively correlated with enhanced disease resistance to bacterialblight. These results suggest that the expression of these DR genes is developmentallycontrolled and regulated by the lesion mimic genes and that mis-regulation ofcertain defense-related genes was correlated with the resistant phenotypes. Severalsubtractive cDNA libraries induced by pathogens have been constructed and a panelof candidate genes is being used to correlate gene expression with broad-spectrumdisease resistance (J. Leach, published data).Sheath blight caused by Rhizoctonia solani is a difficult disease to evaluate becauseof the variability associated with the disease response and the strong environmentalinfluence on pathogen-host interactions. However, there is an urgent need tosearch for endogenous genes that can enhance sheath blight resistance as no geneticresistance has yet been found through conventional screening of rice germplasm. Ourstrategy is to first identify mutants with a gain or loss in resistance to blast and bacte-244 Leung et al