The mutants used in this study includedAK631, an exoB mutant of Rm41 deficient in EPS production (EPS-); PP4709, an rkp1 mutant of RM41 defi- cient in production of KPS (KPS-), and PP674, an rkp1 mutant of AK631 deficient in production of both EPS and KPS (EPS-KPS-) (Table 2). Our data showed that PP4709 (KPS-) behaved similar to the wild-type strain Rm41 and can normally nodulate A20 and DZA045.5, suggesting that KPS production of Rm41 is not required for nodulation with the M. truncatula genotypes A20 and DZA045.5. In contrast, AK631 (ESP-) and PP674 (EPS-KPS-) were not able to nodulate DZA045.5, and AK631 only induced the formation of a few Fix- nodules on the A20 roots, which suggested that EPS production plays an important role in establishing an efficient sym- biosis with M. truncatula and their role can’t be comple- mented by KPS. Our data are consistent with that reported by Simesk et al. [35].
Neither single nor double mutants of Rm41 could nodulate F83005.5, which appears to suggest that the in- compatibility between F83005.5 and Rm41 is not associ- ated with EPS and KPS production. However, we can’t exclude the possibility that EPS is required for nodula- tion in the compatible interaction but also essential for eliciting defense responses in the F83005.5 background. This scenario is similar to the T3SS of pathogenic bac- teria, for which T3SS is required for causing disease in susceptible hosts and for eliciting the hypersensitive re- sponse in resistant hosts, and defects in the T3SS ren- ders a bacterium non-pathogenic [45].