Rice Genetics IV - IRRI books - International Rice Research Institute

IRBB2134532703506N20-247N18-116-1N18-238-1RearrangementDeletionFig. 3. Polymerase chain reaction analysis of putative mutants using the Xa21 leucine-richrepeat-specific primers. DEB mutants are 3453, 270, and 3506; N20-247, N18-116-1, andN18-238-1 are fast-neutron mutants.the LRR region showed only one hybridizing band. Interestingly, all these 10 linesthat had deletions in the Xa21 gene cluster were highly susceptible to Xoo. Mutantswith partial resistance to race 6 had no apparent deletion in the Xa21 locus, whichwas detected based upon both PCR and Southern analyses, suggesting that thesemutations occur at other loci controlling the Xa21-mediated defense pathway.To investigate whether the resistance pathway mediated by the Xa21 gene is sharedwith the pathways required by the genes with resistance to blast, all mutants wereinoculated with four Philippine blast isolates belonging to four different genetic lineages.Most of the lines showed no difference in their resistance specificity to all theisolates except lines 3453, 3469, and N20-247, which were susceptible to two out ofseven blast isolates that are incompatible to IRBB21. Interestingly, all three lineshave deletions in the Xa21 locus.Crosses were made between these three mutant lines and the wild-type IRBB21.The F 2 families were used to determine whether the Xa21 gene confers a dual-resistancefunction (to bacterial blight and blast). After inoculation with blast isolate PO6-6, DNA was extracted from at least 50 individual plants for genotype analysis. BothPCR and Southern blot methods are used in the analysis. In all three F 2 families, nocorrelation was observed between the absence of the Xa21 gene and blast susceptibilityof individual plants. However, phenotypic and molecular analyses of the F 2 familiesshow that susceptibility to two bacterial blight strains (PXO79 and PXO99) cosegregatesperfectly with the Xa21 deletion. These results indicate that bacterial blightand blast susceptibility in these three mutants are completely independent.Structure, function, and evolution of disease resistance . . . 341