Abstract
Xa3-mediated resistance for rice bacterial blight, one of the most devastating rice diseases worldwide, is influenced by genetic background. Xa3 is genetically tightly linked to Xa26, another gene for bacterial blight resistance. Xa26 belongs to a clustered multigene family encoding leucine-rich repeat (LRR) receptor kinase-like proteins. To characterize Xa3, we fine mapped it using a population segregating for only one resistance gene and markers developed from Xa26 family. Genetic analysis showed that Xa3 co-segregated with the marker of Xa26 gene and segregated from the markers of other members of Xa26 family. DNA fingerprinting revealed that rice line IRBB3 carrying Xa3 had the same copy numbers of Xa26 family members as rice line Minghui 63 carrying Xa26. Phenotypic comparison showed that all the rice lines carrying either Xa3 or Xa26 developed dark brown deposition at the border between the lesion caused by incompatible-pathogen infection and health leaf tissue, while other rice lines did not show this dark brown deposition in either incompatible or compatible interactions. These results suggest that Xa3 and Xa26 is the same gene. We name it Xa3/Xa26 to indicate the relationship between the two gene symbols. The putative encoding products of Xa3/Xa26 and its susceptible allele xa3/xa26 shared 92% sequence identity. The sequence difference occurred in the LRR domains, specifically at the solvent-exposed amino acid residues, might be the major cause that differentiates the resistant and susceptible proteins.
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Acknowledgments
We thank the International Rice Research Institute for providing the rice near isogenic lines of bacterial blight resistance and the Philippine strains of Xoo. This work was supported by grants from the National Program on the Development of Basic Research in China and the National Natural Science Foundation of China.
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Xiang, Y., Cao, Y., Xu, C. et al. Xa3, conferring resistance for rice bacterial blight and encoding a receptor kinase-like protein, is the same as Xa26 . Theor Appl Genet 113, 1347–1355 (2006). https://doi.org/10.1007/s00122-006-0388-x
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DOI: https://doi.org/10.1007/s00122-006-0388-x