Abstract
Bradyrhizobium elkanii USDA61 possesses a functional type III secretion system (T3SS) that controls host-specific symbioses with legumes. Here, we demonstrated that B. elkanii T3SS is essential for the nodulation of several southern Asiatic Vigna mungo cultivars. Strikingly, inactivation of either Nod factor synthesis or T3SS in B. elkanii abolished nodulation of the V. mungo plants. Among the effectors, NopL was identified as a key determinant for T3SS-dependent symbiosis. Mutations of other effector genes, such as innB, nopP2, and bel2-5, also impacted symbiotic effectiveness, depending on host genotypes. The nopL deletion mutant formed no nodules on V. mungo, but infection thread formation was still maintained, thereby suggesting its pivotal role in nodule organogenesis. Phylogenetic analyses revealed that NopL was exclusively conserved among Bradyrhizobium and Sinorhizobium (Ensifer) species and showed a different phylogenetic lineage from T3SS. These findings suggest that V. mungo evolved a unique symbiotic signaling cascade that requires both NFs and T3Es (NopL).
Highlights
Bacteria have continuously evolved a multitude of strategies to promote infections in their hosts, including the direct injection of proteins via protein secretion systems
We previously reported that T3SS of B. elkanii USDA61 abolished V. radiata nodulation but highly promoted symbiosis with V. mungo, suggesting its important roles in controlling host-species-specific symbiotic interactions [9]
Inactivation of nopL excluded nodulation on IBPGR2775-3 and MASH (Figures 1 and 2) but largely reduced nodule numbers of PI173934 (Figure S3). These results suggest that USDA61 NopL, possibly together with other T3Es, suppresses MAPK-triggered responses and/or modulates NF-dependent symbiosis signaling toward determining the nodulation of
Summary
Bacteria have continuously evolved a multitude of strategies to promote infections in their hosts, including the direct injection of proteins via protein secretion systems. Numerous Gram-negative pathogenic bacteria employ a type III secretion system (T3SS) to translocate their virulence effector proteins (hereafter T3Es) directly into host cells to promote infection and pathogenesis [1]. Rhizobial T3SS-secreted proteins, called nodulation outer proteins (Nops), are injected into host cells as T3Es depending on an extracellular secretion apparatus [7]. Some T3Es modulate host functions toward promoting infection and symbiosis with legumes [6], while several T3Es may be recognized as asymbiotic factors directly or indirectly via host resistance (R) proteins or specific receptors, triggering immune responses that restrict nodulation [7].
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