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| In this study, we established a system in which host plants, bacterial pathogens, and symbiont rhizobia are included to study the role of innate immunity during symbiotic interactions. A pathogenic bacterium, Pseudomonas syringae pv. Tomato strain DC3000 (Pst DC3000) was found to cause chlorosis on leaves of Medicago truncatula A17. It was found that Sinorhizobium meliloti Sm2011 strain (Sm2011) and Pst DC3000 strain induce similar defense responses in M. truncatula, and symbiotic bacterium S. meliloti Sm2011 specific suppressed the defense responses that induced by pathogen of Pst DC3000. Inoculation with S. meliloti Sm2011 suppresses the transcription of defense-related genes including receptor of bacterial flagellin (FLS2), pathogenesis-related protein 10 (PR10) and transcription factors WRKY33 triggered by Pst DC3000 infection. Interestingly, treatment with Pst DC3000 was shown to specially inhibit the expression of symbiosis marker genes nodule inception (NIN) and nodulation pectate lyase (NPL) and to reduce the infection threads and nodules numbers on M. truncatula A17 roots, indicated that Pst DC3000 inhibits the establishment of symbiosis in M. truncatula. In addition, defense-related genes, such as MAPK3/6, RbohC and WRKY33 exhibit a transient increase in their expressions in the early stage of symbiosis, but drop down to normal level during symbiotic nitrogen fixation with strain S. meliloti Sm2011. Our data suggest that plant innate immunity plays an antagonistic role with symbiosis by directly inhibiting the formation of infection thread and nodule numbers. |
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| Keywords:Medicago truncatula; Sinorhizobium meliloti Sm2011; Pseudomonas syringae pv. tomato DC3000; defense response; symbiosis |
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