Genetic and Molecular Dissection of Blast Resistance in Rice Using RFLP, Simple Sequence Repeats and Defense-Related Candidate Gene Markers

Abstract

Blast, Pyricularia grisea (Cooke) Sacc., is one of the most destructive diseases of rice worldwide and can<br />result in significant reductions in yield. The use of resistant cultivars is the most economical and effective<br />way of controlling rice blast. A variety of DNA markers, including plant defense-related candidate<br />gene markers are available for genetic characterization and molecular analysis of rice. A set of 161<br />recombinant inbred lines, RILs, from a cross between Nemat, an improved and high yielding cultivar, and<br />Anbarboo, a traditional and aromatic rice, was used to identify defense-related candidate gene, RFLP<br />and SSR markers linked to components of resistance to blast, i.e. infection type, lesion density, the percent<br />of diseased leaf area, and lesion size in rice. The RILs were tested using two single blast isolates in<br />greenhouse, and field population of blast in blast nursery in International Rice Research Institute,<br />Philippines, in 2000–2001. Of the 86 defense-related candidate gene, 153 RFLP, and SSR markers 26<br />defense-related candidate gene, 66 RFLP, and 85 SSR markers were polymorphic in two parental lines.<br />Results showed that a defense gene, b8, a NBS-LRR originated from barley, closely linked to different components of resistance to blast. The defense genes of r5, r7, PrP2, and ERS from rice, maize, and<br />Arabidopsis, respectively, have had minor effects on different components of resistance to blast. The<br />RFLP markers, i.e. RZ536, RG351, RZ76, RZ397 on chromosomes 7, 11 and 12, and the SSR markers<br />including RM224, RM179, and RM277 on chromosomes 11 and 12 were tightly linked to componentsof resistance to blast. The linked markers can now be used for resistance gene pyramiding and markerassisted<br />selection in the breeding population. The results suggested the presence of race-specific resistance<br />genes exhibiting strong differential pathogenhost interaction. We need to incorporate new sources of gene pool to make the genetic base broaden.<br /><br />