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How plants deal with beneficial and pathogenic microorganisms and how they can tolerate beneficial ones and face pathogens at the same time are questions that remain puzzling to plant biologists. Legume plants are good models to explore those issues, as their interactions with nitrogen-fixing bacteria called rhizobia results in a drastic and easy-to-follow phenotype of nodulation. Intriguingly, despite massive and chronic infection, legume defense reactions are essentially suppressed during the whole symbiotic process, raising a question about a potential negative effect of plant immune responses on the establishment of nodulation. In the present study, we used the model legume, Medicago truncatula , coinoculated with mutualistic and phytopathogenic bacteria, Sinorhizobium medicae and Ralstonia solanacearum , respectively. We show that the presence of R. solanacearum drastically inhibits the nodulation process. The type III secretion system of R. solanacearum , which is important for the inhibition of pathogen-associated molecular pattern-triggered immunity (PTI), strongly contributes to inhibit nodulation. Thus, our results question the negative effect of PTI on nodulation. By including a pathogenic bacterium in the interaction system, our study provides a new angle to address the influence of the biotic environment on the nodulation process.[Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

In symbiotic root nodules of legumes, terminally differentiated rhizobia fix atmospheric N2 producing an NH4+ influx that is assimilated by the plant. The plant, in return, provides photosynthates that fuel the symbiotic nitrogen acquisition. Mechanisms responsible for the adjustment of the symbiotic capacity to the plant N demand remain poorly understood. We have investigated the role of systemic signaling of whole-plant N demand on the mature N2-fixing nodules of the model symbiotic association Medicago truncatula/Sinorhizobium using split-root systems. The whole-plant N-satiety signaling rapidly triggers reductions of both N2 fixation and allocation of sugars to the nodule. These responses are associated with the induction of nodule senescence and the activation of plant defenses against microbes, as well as variations in sugars transport and nodule metabolism. The whole-plant N-deficit responses mirror these changes: a rapid increase of sucrose allocation in response to N-deficit is associated with a stimulation of nodule functioning and development resulting in nodule expansion in the long term. Physiological, transcriptomic, and metabolomic data together provide evidence for strong integration of symbiotic nodules into whole-plant nitrogen demand by systemic signaling and suggest roles for sugar allocation and hormones in the signaling mechanisms., (© The Author(s) 2020. Published by Oxford University Press on behalf of the Society for Experimental Biology.)

In ST-segment elevation myocardial infarction of both patients and mice, there was a decline in blood eosinophil count, with activated eosinophils recruited to the infarct zone. Eosinophil deficiency resulted in attenuated anti-inflammatory macrophage polarization, enhanced myocardial inflammation, increased scar size, and deterioration of myocardial structure and function. Adverse cardiac remodeling in the setting of eosinophil deficiency was prevented by interleukin-4 therapy., (© 2020 The Authors.)

Legumes have the capacity to develop root nodules hosting nitrogen-fixing bacteria, called rhizobia. For the plant, the benefit of the symbiosis is important in nitrogen-deprived conditions, but it requires hosting and feeding massive numbers of rhizobia. Recent studies suggest that innate immunity is reduced or suppressed within nodules [1-10]; this likely maintains viable rhizobial populations. To evaluate the potential consequences and risks associated with an altered immuni`ty in the symbiotic organ, we developed a tripartite system with the model legume Medicago truncatula [11, 12], its nodulating symbiont of the genus Sinorhizobium (syn. Ensifer) [13, 14], and the pathogenic soil-borne bacterium Ralstonia solanacearum [15-18]. We show that nodules are frequent infection sites where pathogen multiplication is comparable to that in the root tips and independent of nodule ability to fix nitrogen. Transcriptomic analyses indicate that, despite the presence of the hosted rhizobia, nodules are able to develop weak defense reactions against pathogenic R. solanacearum. Nodule defense response displays specificity compared to that activated in roots. In agreement with nodule innate immunity, optimal R. solanacearum growth requires pathogen virulence factors. Finally, our data indicate that the high susceptibility of nodules is counterbalanced by the existence of a diffusion barrier preventing pathogen spreading from nodules to the rest of the plant., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Rhizobia display dual lifestyle. These bacteria are soil inhabitants but can also elicit the formation of a special niche on the root of legume plants, the nodules. In such organs, rhizobia can promote the growth of their host by providing them nitrogen they captured from atmosphere. All along the infection process, the plant innate immunity has to be controlled to maintain compatible interaction. However, nodulation does not always result in profit for the plant as compatible interactions include both nitrogen-fixing and non-fixing associations. In recent years, our knowledge on the mechanisms involved in the control of plant innate immunity during rhizobia-legume interactions has greatly improved notably by the identification of bacterial and plant genes activating or suppressing the plant defences. Surprisingly, results also demonstrated that in some cases, plant defence reactions result in abortion of the nodulation process despite that the rhizobial strain has all the genetic potential to establish mutualism. In such situation, experimental evolution approaches highlighted possible rapid switches of incompatible rhizobia either to mutualistic or parasitic behaviour. Here, we review this recent literature., (© 2019 John Wiley & Sons Ltd.)