Regulation by oxygen (O2) in rhizobia is essential for their symbioses with plants and involves multiple O2 sensing proteins. Three sensors exist in the pea microsymbiont Rhizobium leguminosarum Rlv3841: hFixL, FnrN and NifA. At low O2 concentrations (1%) hFixL signals via FxkR to induce expression of the FixK transcription factor, which activates transcription of downstream genes. These include fixNOQP, encoding the high-affinity cbb3-type terminal oxidase used in symbiosis. In free-living Rlv3841, the hFixL-FxkR-FixK pathway was active at 1% O2, and confocal microscopy showed hFixL-FxkR-FixK activity in the earliest stages of Rlv3841 differentiation in nodules (zones I and II). Work on Rlv3841 inside and outside nodules showed that the hFixL-FxkR-FixK pathway also induces transcription of fnrN at 1% O2 and in the earliest stages of Rlv3841 differentiation in nodules. We confirmed past findings suggesting a role for FnrN in fixNOQP expression. However, unlike hFixL-FxkR-FixK, Rlv3841 FnrN was only active in the near-anaerobic zones III and IV of pea nodules. Quantification of fixNOQP expression in nodules showed this was driven primarily by FnrN, with minimal direct hFixL-FxkR-FixK induction. Thus, FnrN is key for full symbiotic expression of fixNOQP. Without FnrN, nitrogen fixation was reduced by 85% in Rlv3841, while eliminating hFixL only reduced fixation by 25%. The hFixL-FxkR-FixK pathway effectively primes the O2 response by increasing fnrN expression in early differentiation (zones I-II). In zone III of mature nodules, near-anaerobic conditions activate FnrN, which induces fixNOQP transcription to the level required for wild-type nitrogen fixation activity. Modelling and transcriptional analysis indicates that the different O2 sensitivities of hFixL and FnrN lead to a nuanced spatiotemporal pattern of gene regulation in different nodule zones in response to changing O2 concentration. Multi-sensor O2 regulation is prevalent in rhizobia, suggesting the fine-tuned control this enables is common and maximizes the effectiveness of the symbioses.
bResistance to the innate defenses of the intestine is crucial for the survival and carriage of Staphylococcus aureus, a common colonizer of the human gut. Bile salts produced by the liver and secreted into the intestines are one such group of molecules with potent antimicrobial activity. The mechanisms by which S. aureus is able to resist such defenses in order to colonize and survive in the human gut are unknown. Here we show that mnhF confers resistance to bile salts, which can be abrogated by efflux pump inhibitors. MnhF mediates the efflux of radiolabeled cholic acid both in S. aureus and when heterologously expressed in Escherichia coli, rendering them resistant. Deletion of mnhF attenuated the survival of S. aureus in an anaerobic three-stage continuous-culture model of the human colon (gut model), which represents different anatomical areas of the large intestine. Staphylococcus aureus is a ubiquitous and highly adaptable human pathogen responsible for a significant global burden of morbidity and mortality. The bacterium lives as a commensal in the nares of 20 to 25% of the population at any one time (1, 2). While nasal colonization is a well-established risk factor for most types of S. aureus infections, several recent studies have suggested that colonization of the intestine, which occurs in ca. 20% of individuals and which by and large has been overlooked, could have important clinical implications (3). Patients with S. aureus intestinal colonization can serve as an important source of transmission, as they often contaminate the adjacent environment (4). Similarly, such patients display an increased frequency of skin colonization (5). A study of intensive care and liver transplant units showed that patients with both rectal and naris colonization by methicillin-resistant S. aureus (MRSA) had a significantly higher risk of disease (40%) than did patients with nasal colonization alone (18%) (6). Furthermore, a study of hospitalized patients in the United States reported cocolonization by S. aureus and vancomycin-resistant enterococci in Ͼ50% of the individuals studied (7). Thus, it is likely that intestinal colonization by S. aureus provides the pathogen a potential opportunity to acquire new antibiotic resistance genes.While the clinical implications of intestinal colonization by S. aureus are still relatively ill defined, it is assumed that carriage is a risk for intestinal infection; S. aureus can induce pseudomembranous colitis that is histologically distinct from that caused by Clostridium difficile (8). Multiple studies have demonstrated frequent intestinal colonization in infants, particularly those who were breast fed, and that there is a positive correlation with the development of allergies (9-13). While a role for S. aureus intestinal carriage in the development of systemic S. aureus disease has not been established, colonization of the intestinal lumen of mice can lead to the pathogen crossing the intestinal epithelial barrier and subsequently spreading to the mesenteric lymph nodes (14, 15)...
Summary Rhizobium leguminosarum has two high‐affinity Mn2+ transport systems encoded by sitABCD and mntH. In symbiosis, sitABCD and mntH were expressed throughout nodules and also strongly induced in Mn2+‐limited cultures of free‐living cells. Growth of a sitA mntH double mutant was severely reduced under Mn2+ limitation and sitA and mntH single mutants were more sensitive to oxidative stress. The double sitA mntH mutant of R. leguminosarum was unable to fix nitrogen (Fix‐) with legumes belonging to the galegoid clade (Pisum sativum, Vicia faba and Vicia hirsuta). The presence of infection thread‐like structures and sparsely‐packed plant cells in nodules suggest that bacteroid development was blocked, either at a late stage of infection thread progression or during bacteroid‐release. In contrast, a double sitA mntH mutant was Fix+ on common bean (Phaseoli vulgaris), a member of the phaseoloid clade of legumes, indicating a host‐specific symbiotic requirement for Mn2+ transport.
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