Bacterial leaf streak 1 encoding a mitogen-activated protein kinase confers resistance to bacterial leaf streak in rice

Bacterial leaf streak (BLS) is a major bacterial disease of rice. Utilization of host genetic resistance has become one of the most important strategies for controlling BLS. However, only a few resistance genes have been characterized. Previously, a recessive BLS resistance gene bls1 was roughly mapped on chromosome 6. Here, we further delineated bls1 to a 21 kb region spanning four genes. Genetic analysis confirmed that the gene encoding a mitogen-activated protein kinase (OsMAPK6) is the target of the allelic genes BLS1 and bls1. Overexpression of BLS1 weakened resistance to the specific Xanthomonas oryzae pv. oryzicola (Xoc) strain JZ-8, while low expression of bls1 increased resistance. However, both overexpression of BLS1 and low expression of bls1 could increase no-race-specific broad-spectrum resistance. These results indicate that BLS1 and bls1 negatively regulate race-specific resistance to Xoc strain JZ-8 but positively and negatively control broad-spectrum resistance, respectively. Subcellular localization demonstrated that OsMAPK6 was localized in the nucleus. RGA4, which is known to mediate resistance to Xoc, is the potential target of OsMAPK6. Overexpression of BLS1 and low expression of bls1 showed increase in salicylic acid and induced expression of defense-related genes, simultaneously increasing broad-spectrum resistance. Moreover, low expression of bls1 showed increase an in jasmonic acid and abscisic acid, in company with an increase in resistance to Xoc strain JZ-8. Collectively, our study provides new insights into the understanding of BLS resistance and facilitates the development of rice host-resistant cultivars.

Automated summary

This study further delineated the location and mechanism of the recessive BLS resistance gene bls1 in rice, indicating that OsMAPK6 is its target gene, regulating resistance to the Xoc strain JZ-8. BLS1 and bls1 negatively regulate resistance to specific strains while positively and negatively controlling broad-spectrum resistance, respectively, by activating defense-related genes.