title: Characterization of rice mutants with enhanced susceptibility to rice blast.
abstract: As a first step towards identifying genes involving in the signal transduction pathways mediating rice blast resistance, we isolated 3 mutants lines that showed enhanced susceptibility to rice blast KJ105 (91-033) from a T-DNA insertion library of the japonica rice cultivar, Hwayeong. Since none of the susceptible phenotypes co-segregated with the T-DNA insertion we adapted a map-based cloning strategy to isolate the gene(s) responsible for the enhanced susceptibility of the Hwayeong mutants. A genetic mapping population was produced by crossing the resistant wild type Hwayeong with the susceptible cultivar, Nagdong. Chi-square analysis of the F2 segregating population indicated that resistance in Hwayeong was controlled by a single major gene that we tentatively named Pi-hy. Randomly selected susceptible plants in the F2 population were used to build an initial map of Pi-hy. The SSLP marker RM2265 on chromosome 2 was closely linked to resistance. High resolution mapping using 105 F2 plants revealed that the resistance gene was tightly linked, or identical, to Pib, a resistance gene with a nucleotide binding sequence and leucine-rich repeats (NB-LRR) previously isolated. Sequence analysis of the Pib locus amplified from three susceptible mutants revealed lesions within this gene, demonstrating that the Pi-hy gene is Pib. The Pib mutations in 1D-22-10-13, 1D-54-16-8, and 1C-143-16-1 were, respectively, a missense mutation in the conserved NB domain 3, a nonsense mutation in the 5th LRR, and a nonsense mutation in the C terminus following the LRRs that causes a small deletion of the C terminus. These findings provide evidence that NB domain 3 and the C terminus are required for full activity of the plant R gene. They also suggest that alterations of the resistance gene can cause major differences in pathogen specificity by affecting interactions with an avirulence factor.
authors.affiliation: Plant Metabolism Research Center and Graduate School of Biotechnology, Kyung Hee University, Yongin 449-701, Korea.
authors.forename: Hye-Kyung
authors.initials: HK
authors.lastname: Kim
authors.forename: Sang-Kyu
authors.initials: SK
authors.lastname: Lee
authors.forename: Jung-Il
authors.initials: JI
authors.lastname: Cho
authors.forename: Sichul
authors.initials: S
authors.lastname: Lee
authors.forename: Gynheung
authors.initials: G
authors.lastname: An
authors.forename: Nam-Soo
authors.initials: NS
authors.lastname: Jwa
authors.forename: Byung-Ryun
authors.initials: BR
authors.lastname: Kim
authors.forename: Young-Chan
authors.initials: YC
authors.lastname: Cho
authors.forename: Seong-Sook
authors.initials: SS
authors.lastname: Han
authors.forename: Seong-Hee
authors.initials: SH
authors.lastname: Bhoo
authors.forename: Youn-Hyung
authors.initials: YH
authors.lastname: Lee
authors.forename: Yeon-Kyu
authors.initials: YK
authors.lastname: Hong
authors.forename: Gihwan
authors.initials: G
authors.lastname: Yi
authors.forename: Dae-Sup
authors.initials: DS
authors.lastname: Park
authors.forename: Tae-Ryong
authors.initials: TR
authors.lastname: Hahn
authors.forename: Jong-Seong
authors.initials: JS
authors.lastname: Jeon
mesh_terms: D002352:Carrier Proteins / Q000235:genetics*; D032461:Chromosomes, Plant; D018744:DNA, Plant / Q000235:genetics; D004198:Disease Susceptibility; D005819:Genetic Markers; D007113:Immunity, Innate; D009154:Mutation / Q000235:genetics*; D012275:Oryza / Q000235:genetics* / Q000382:microbiology*; D028044:Phosphate-Binding Proteins; D010935:Plant Diseases / Q000235:genetics* / Q000382:microbiology; D010940:Plant Proteins / Q000235:genetics*; D030821:Plants, Genetically Modified
chemical_list: D002352:Carrier Proteins; D018744:DNA, Plant; D005819:Genetic Markers; D028044:Phosphate-Binding Proteins; C121462:Pib protein, Oryza sativa; D010940:Plant Proteins