MtNAD1 associates with the autophagy complex to contribute to the degradation of immunity-related proteins in Medicago truncatula nodules

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.