경희대학교 식물기능유전체학 실험실

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AUTHOR

H-K Kim, S-K Lee, J-I Cho, S Lee, G An, N-S Jwa, B-R Kim, Y-C Cho, S-S Han, S-H Bhoo, Y-H Lee, Y-K Hong, G Yi, D-S Park, T-R Hahn, J-S Jeon (2005)

TITLE

Characterization of rice mutants with enhanced disease susceptibility to rice blast

JOURNAL

Mol Cells, 20(30): 375-381

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The Abstract Of The Paper

As a first step towards identifying genes involving in the signal transduction pathways mediating rice blast resistance, we isolated 3 rice mutants lines that showed enhanced susceptibility to invading rice blast KJ105 (91-033), from the T-DNA insertion mutant population of a japonica rice cultivar, Hwayeong. Since none of the susceptible phenotypes were co-segregated with T-DNA insertions, we adapted a map-based cloning strategy to isolate a causal gene responsible for the enhanced susceptibility of the Hwayeong mutants, since this cultivar is generally resistant to rice blast. A genetic mapping population was produced by crossing the resistant wild-type Hwayeong with a susceptible cultivar, Nagdong. Chi-square analysis of the F2 segregating population indicated that resistance in Hwayeong is controlled by a single major gene, which we tentatively named Pi-hy. Randomly selected susceptible plants in the F2 population were first used to build an initial map of Pi-hy. Among tested SSLP markers, RM2265 positioned on chromosome 2 was closely linked to resistance. High resolution mapping analysis using 105 F2 plants revealed that the resistance gene is tightly linked with, or is the same gene as, Pib, an NB-LRR (nucleotide binding sequence and leucine-rich repeats) resistance gene that was isolated previously. Sequence analysis of the Pib locus amplified from three susceptible mutants identified lesions within this resistance 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 include a missense mutation in the NB conserved 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 in the C terminus, respectively. This provides evidence that the NB domain 3 and C terminus are functionally required for full activity of the plant R gene. Finally, our results suggest that variations in the resistance gene cause major differences in pathogen specificity by altering interactions with an avirulence factor.

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