Rhizobial lipochitooligosaccharidic Nod factors (NFs), specified by We examined the nodulation ability of We show that the Our findings reveal that a newly evolved gene in R108,
- Award ID(s):
- 1645590
- NSF-PAR ID:
- 10321288
- Editor(s):
- Stabb, Eric V.
- Date Published:
- Journal Name:
- Applied and Environmental Microbiology
- Volume:
- 87
- Issue:
- 15
- ISSN:
- 0099-2240
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Summary nod genes, are the primary determinants of host specificity in the legume–Rhizobia symbiosis.Medicago truncatula cv Jemalong A17 andM. truncatula ssp.tricycla R108 with theSinorhizobium meliloti nodF/nodL mutant, which produces modified NFs. We then applied genetic and functional approaches to study the genetic basis and mechanism of nodulation of R108 by this mutant.nodF/nodL mutant can nodulate R108 but not A17. Using genomics and reverse genetics, we identified a newly evolved, chimeric LysM receptor‐like kinase gene in R108,LYK2bis , which is responsible for the phenotype and can allow A17 to gain nodulation with thenodF/nodL mutant. We found thatLYK2bis is involved in nodulation by mutants producing nonO ‐acetylated NFs and interacts with the key receptor protein NFP. Many, but not all, naturalS. meliloti andS. medicae strains tested requireLYK2bis for efficient nodulation of R108.LYK2bis , extends nodulation specificity to mutants producing nonO ‐acetylated NFs and is important for nodulation by many naturalSinorhizobia . Evolution of this gene may present an adaptive advantage to allow nodulation by a greater variety of strains. -
Premise Polyploidy is a major genetic driver of ecological and evolutionary processes in plants, yet its effects on plant interactions with mutualistic microbes remain unresolved. The legume–rhizobium symbiosis regulates global nutrient cycles and plays a role in the diversification of legume species. In this mutualism, rhizobia bacteria fix nitrogen in exchange for carbon provided by legume hosts. This exchange occurs inside root nodules, which house bacterial cells and represent the interface of legume–rhizobium interactions. Although polyploidy may directly impact the legume–rhizobium mutualism, no studies have explored how it alters the internal structure of nodules.
Methods We created synthetic autotetraploids using
Medicago sativa subsp.caerulea . Neotetraploid plants and their diploid progenitors were singly inoculated with two strains of rhizobia,Sinorhizobium meliloti andS. medicae . Confocal microscopy was used to quantify internal traits of nodules produced by diploid and neotetraploid plants.Results Autotetraploid plants produced larger nodules with larger nitrogen fixation zones than diploids for both strains of rhizobia, although the significance of these differences was limited by power. Neotetraploid
M. sativa subsp.caerulea plants also produced symbiosomes that were significantly larger, nearly twice the size, than those present in diploids.Conclusions This study sheds light on how polyploidy directly affects a plant–bacterium mutualism and uncovers novel mechanisms. Changes in plant–microbe interactions that directly result from polyploidy likely contribute to the increased ability of polyploid legumes to establish in diverse environments.
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Abstract In the legume‐rhizobia mutualism, the benefit each partner derives from the other depends on the genetic identity of both host and rhizobial symbiont. To gain insight into the extent of genome × genome interactions on hosts at the molecular level and to identify potential mechanisms responsible for the variation, we examined host gene expression within nodules (the plant organ where the symbiosis occurs) of four genotypes of
Medicago truncatula grown with eitherEnsifer meliloti orE. medicae symbionts. These host × symbiont combinations show significant variation in nodule and biomass phenotypes. Likewise, combinations differ in their transcriptomes: host, symbiont and host × symbiont affected the expression of 70%, 27% and 21%, respectively, of the approximately 27,000 host genes expressed in nodules. Genes with the highest levels of expression often varied between hosts and/or symbiont strain and include leghemoglobins that modulate oxygen availability and hundreds of Nodule Cysteine‐Rich (NCR ) peptides involved in symbiont differentiation and viability in nodules. Genes with host × symbiont‐dependent expression were enriched for functions related to resource exchange between partners (sulphate/iron/amino acid transport and dicarboxylate/amino acid synthesis). These enrichments suggest mechanisms for host control of the currencies of the mutualism. The transcriptome ofM. truncatula accessionHM 101 (A17), the reference genome used for most molecular research, was less affected by symbiont identity than the other hosts. These findings underscore the importance of assessing the molecular basis of variation in ecologically important traits, particularly those involved in biotic interactions, in multiple genetic contexts. -
Summary The formation of nitrogen‐fixing nodules on legume hosts is a finely tuned process involving many components of both symbiotic partners. Production of the exopolysaccharide succinoglycan by the nitrogen‐fixing bacterium
Sinorhizobium meliloti 1021 is needed for an effective symbiosis withMedicago spp., and the succinyl modification to this polysaccharide is critical. However, it is not known when succinoglycan intervenes in the symbiotic process, and it is not known whether the plant lysin‐motif receptor‐like kinase MtLYK10 intervenes in recognition of succinoglycan, as might be inferred from work on theLotus japonicus MtLYK10 ortholog, LjEPR3. We studied the symbiotic infection phenotypes ofS. meliloti mutants deficient in succinoglycan production or producing modified succinoglycan, in wild‐typeMedicago truncatula plants and inMtlyk10 mutant plants. On wild‐type plants,S. meliloti strains producing no succinoglycan or only unsuccinylated succinoglycan still induced nodule primordia and epidermal infections, but further progression of the symbiotic process was blocked. TheseS. meliloti mutants induced a more severe infection phenotype onMtlyk10 mutant plants. Nodulation by succinoglycan‐defective strains was achieved byin trans rescue with a Nod factor‐deficientS. meliloti mutant. While the Nod factor‐deficient strain was always more abundant inside nodules, the succinoglycan‐deficient strain was more efficient than the strain producing only unsuccinylated succinoglycan. Together, these data show that succinylated succinoglycan is essential for infection thread formation inM. truncatula , and that MtLYK10 plays an important, but different role in this symbiotic process. These data also suggest that succinoglycan is more important than Nod factors for bacterial survival inside nodules. -
Plants have evolved the ability to distinguish between symbiotic and pathogenic microbial signals. However, potentially cooperative plant–microbe interactions often abort due to incompatible signaling. The Nodulation Specificity 1 ( NS1 ) locus in the legume Medicago truncatula blocks tissue invasion and root nodule induction by many strains of the nitrogen-fixing symbiont Sinorhizobium meliloti . Controlling this strain-specific nodulation blockade are two genes at the NS1 locus, designated NS1a and NS1b , which encode malectin-like leucine-rich repeat receptor kinases. Expression of NS1a and NS1b is induced upon inoculation by both compatible and incompatible Sinorhizobium strains and is dependent on host perception of bacterial nodulation (Nod) factors. Both presence/absence and sequence polymorphisms of the paired receptors contribute to the evolution and functional diversification of the NS1 locus. A bacterial gene, designated rns1 , is required for activation of NS1 -mediated nodulation restriction. rns1 encodes a type I-secreted protein and is present in approximately 50% of the nearly 250 sequenced S. meliloti strains but not found in over 60 sequenced strains from the closely related species Sinorhizobium medicae . S. meliloti strains lacking functional rns1 are able to evade NS1 -mediated nodulation blockade.more » « less