Abstract

Plant immunity is suppressed in the symbiotic nodule cells, thereby facilitating rhizobial infection. Medicago truncatula NODULES WITH ACTIVATED DEFENSE1 (MtNAD1) is crucial for suppressing immunity in nodules; however, its molecular function is unclear. We explored the molecular basis of the role of MtNAD1 in suppressing innate immunity in M. truncatula nodules. Medicago truncatula mutants lacking MtATG7 produced defective nodules, sharing some similarities with the Mtnad1 mutant nodules. Furthermore, MtNAD1 interacted with several immunity-related proteins, including BAX-inhibitor1a (MtBI-1a), two Lysin-motif proteins (MtLYM1/2), Pathogenesis-related10 (MtPR10c/d), MtMPK3/6, and two Lysin-motif receptor kinases (MtLYK8/9). In addition, MtNAD1 and the autophagy pathway contributed to the reduction of MtBI-1, MtPR10c/d, and MtLYM1/2 protein levels in planta. Knocking out either the MtBI-1 or MtLYM1/2 gene in the M. truncatula nad1 mutant can partially restore the defective nodules of the nad1 mutant. Our results demonstrate that MtNAD1 associates with the autophagy pathway by interacting with MtATG8, contributing to the degradation of several immunity-related proteins in M. truncatula nodules during rhizobial colonization and thereby supporting the development of a successful symbiosis.

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