A newly-evolved chimeric lysin motif receptor-like kinase in Medicago truncatula spp. tricycla R108 extends its Rhizobia symbiotic partnership

Abstract

SummaryRhizobial lipochitooligosaccharidic Nod factors, specified by nod genes, are the primary determinants of host specificity in the legume-Rhizobia symbiosis. A Sinorhizobium meliloti nodF/nodL mutant produces Nod factors that differ from wild-type ones in lacking an O-acetate, and with a different acyl chain on the terminal non-reducing sugar. This mutant is defective in nodulation with various Medicago hosts.We examined the nodulation ability of M. truncatula cv Jemalong A17 and M. truncatula ssp. tricycla R108 with the nodF/nodL mutant. We then applied genetic and functional approaches to study the genetic basis and mechanism of nodulation of R108 by this mutant.We show that the nodF/nodL mutant can nodulate R108 but not A17. Using genomics and reverse genetics, we identified a newly-evolved gene in R108, LYK2bis, which is responsible for the phenotype. Transformation with LYK2bis allows A17 to gain nodulation with the nodF/nodL mutant. We found that LYK2bis is involved in specific NF signalling and interacts with the key receptor protein NFP.Our findings reveal that a newly-evolved gene in R108, LYK2bis, extends nodulation specificity to strains producing non-O-acetylated NFs. Interaction between LYK2bis and NFP provides a means of integrating the nodulation signalling pathways.