The legume-rhizobial symbiosis results in the formation of root nodules that provide an ecological niche for nitrogen-fixing bacteria. However, plant-bacteria genotypic interactions can lead to wide variation in nitrogen fixation efficiency, and it is not uncommon that a bacterial strain forms functional (Fix + ) nodules on one plant genotype but nonfunctional (Fix − ) nodules on another. Host genetic control of this specificity is unknown. We herein report the cloning of the Medicago truncatula NFS1 gene that regulates the fixation-level incompatibility with the microsymbiont Sinorhizobium meliloti Rm41. We show that NFS1 encodes a nodulespecific cysteine-rich (NCR) peptide. In contrast to the known role of NCR peptides as effectors of endosymbionts' differentiation to nitrogen-fixing bacteroids, we demonstrate that specific NCRs control discrimination against incompatible microsymbionts. NFS1 provokes bacterial cell death and early nodule senescence in an allele-specific and rhizobial strain-specific manner, and its function is dependent on host genetic background.legumes | nodulation | nitrogen fixation specificity | symbiosis persistence | NCR peptides P lants of the legume family can supply their own nitrogen needs through symbioses with nitrogen-fixing soil bacteria called rhizobia. This symbiotic interaction commences when the host perceives rhizobial lipo-chitooligosaccharides known as nodulation (Nod) factors and initiates development of nodule primordia that become infected by the rhizobia (1). Infection of most legumes, including the model legume Medicago truncatula, starts in root hairs and involves formation of plant-made tubular structures known as infection threads (2). Infection threads direct bacteria to these primordia, where the rhizobia are released into the cytoplasm of host cells. During this process, the bacteria become surrounded by a host membrane, and these membrane compartments containing rhizobium are named symbiosomes. Subsequently, the rhizobia differentiate into nitrogen-fixing bacteroids (3).The legume-rhizobial symbiosis shows a high level of specificity, occurring at both species and genotypic levels (4, 5). Incompatible interactions at initial stages of the association can block bacterial infection and nodule organogenesis. This incompatibility can be caused by failed Nod factor or exopolysaccharide recognition (6-9) or by induced plant immune responses (9-11). Symbiotic incompatibility also takes place at later stages of nodule development, resulting in the formation of infected but nonfunctional nodules (12,13). This latter situation is well-documented in the Medicago-Sinorhizobium symbiosis, in which the bacteria undergo terminal differentiation (14). We previously screened a core collection of Medicago accessions using multiple Sinorhizobium meliloti strains, evaluating many host-strain combinations (13). In that experiment, ∼40% of the plant-strain combinations produced small, white infected nodules that were defective in nitrogen fixation (Fix − ) whereas only ∼2% resulte...
Plants detect and respond to pathogen invasion with membrane-localized pattern recognition receptors (PRRs), which recognize pathogen-associated molecular patterns (PAMPs) and activate downstream immune responses. Here we report that LORELEI-LIKE GPI-ANCHORED PROTEIN 1 (LLG1), a coreceptor of the receptor-like kinase FERONIA, regulates PRR signaling. In a forward genetic screen for suppressors of (), we identified the point mutation , which suppresses disease resistance but does not affect plant growth and development. The mutants show enhanced susceptibility to various virulent pathogens, indicating that LLG1 has an important role in plant immunity. LLG1 constitutively associates with the PAMP receptor FLAGELLIN SENSING 2 (FLS2) and the elongation factor-Tu receptor, and forms a complex with BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED RECEPTOR KINASE 1 in a ligand-dependent manner, indicating that LLG1 functions as a key component of PAMP-recognition immune complexes. Moreover, LLG1 contributes to accumulation and ligand-induced degradation of FLS2, and is required for downstream innate immunity responses, including ligand-induced phosphorylation of BOTRYTIS-INDUCED KINASE 1 and production of reactive oxygen species. Taken together, our findings reveal that LLG1 associates with PAMP receptors and modulates their function to regulate disease responses. As LLG1 functions as a coreceptor of FERONIA and plays central roles in plant growth and development, our findings indicate that LLG1 participates in separate pathways, and may suggest a potential connection between development and innate immunity in plants.
Many microbes interact with their hosts across a membrane interface, which is often distinct from existing membranes. Understanding how this interface acquires its identity has significant implications. In the symbiosis between legumes and rhizobia, the symbiosome encases the intracellular bacteria and receives host secretory proteins important for bacterial development. We show that the Medicago truncatula SYNTAXIN 132 (SYP132) gene undergoes alternative cleavage and polyadenylation during transcription, giving rise to two target-membrane soluble NSF attachment protein receptor (t-SNARE) isoforms. One of these isoforms, SYP132A, is induced during the symbiosis, is able to localize to the peribacteroid membrane, and is required for the maturation of symbiosomes into functional forms. The second isoform, SYP132C, has important functions unrelated to symbiosis. The SYP132A sequence is broadly found in flowering plants that form arbuscular mycorrhizal symbiosis, an ancestral mutualism between soil fungi and most land plants. SYP132A silencing severely inhibited arbuscule colonization, indicating that SYP132A is an ancient factor specifying plant-microbe interfaces.
SUMMARYENHANCED DISEASE RESISTANCE 1 (EDR1) is a negative regulator of powdery mildew resistance, cell death and ethylene-induced senescence. To identify components involved in EDR1 signaling, we performed a forward genetic screen for edr1 suppressors. In this screen, we identified the hpr1-4 mutation, which partially suppresses edr1-mediated resistance to the powdery mildew pathogen Golovinomyces cichoracearum and mildew-induced cell death. However, the hpr1-4 mutation enhanced the ethylene-induced senescence phenotype of edr1. The hpr1-4 single mutant displayed enhanced susceptibility to the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 and the oomycete pathogen Hyaloperonospora arabidopsidis Noco2. Arabidopsis HPR1 encodes a homolog of human HPR1, a component of the conserved THO/ transcription export (THO/TREX) complex that is required for mRNA export in yeast and humans. HPR1 is expressed in various organs and throughout all developmental stages. HPR1 localizes to the nucleus, and, significantly, mRNA export is compromised in the hpr1-4 mutant. Taken together, these data demonstrate that HPR1 plays an important role in disease resistance in plants, and that the THO/TREX complex is functionally conserved among plants, yeast and humans. Our data indicate a general link between mRNA export, defense responses and ethylene signaling in plants.
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