Responsiveness of Durum Wheat to Mycorrhizal Inoculation Under Different Environmental Scenarios

A greater understanding of how climate change will affect crop photosynthetic performance has been described as a target goal to improve yield potential. Other concomitant stressors can reduce the positive effect of elevated atmospheric CO₂ on wheat yield. Arbuscular mycorrhizal fungi (AMF) are symbiotic fungi predicted to be important in defining plant responses to rising atmospheric CO₂, but their role in response to global climatic change is still poorly understood. This study aimed to assess if increased atmospheric CO₂ interacting with drought can modify the effects of mycorrhizal symbiosis on flag leaf physiology in winter wheat. The study was performed in climate-controlled greenhouses with ambient (400 ppm, ACO₂) or elevated (700 ppm, ECO₂) CO₂ concentrations in the air. Within each greenhouse half of the plants were inoculated with Rhizophagus intraradices. When ear emergence began, half of the plants from each mycorrhizal and CO₂ treatment were subjected to terminal drought. At ACO₂ AMF improved the photochemistry efficiency of PSII compared with non-mycorrhizal plants, irrespective of irrigation regime. Mycorrhizal wheat accumulated more fructan than non-mycorrhizal plants under optimal irrigation. The level of proline in the flag leaf increased only in mycorrhizal wheat after applying drought. Mycorrhizal association avoided photosynthetic acclimation under ECO₂. However, nitrogen availability to flag leaves in mycorrhizal plants was lower under ECO₂ than at ACO₂. Results suggest that the mechanisms underlying the interactions between mycorrhizal association and atmospheric CO₂ concentration can be crucial for the benefits that this symbiosis can provide to wheat plants undergoing water deficit.     

Bacterial metabolism and pathogenesis intimate intertwining: time for metabolic modelling to come into action

We take a snapshot of the recent understanding of bacterial metabolism and the bacterial‐host metabolic interplay during infection, and highlight key outcomes and challenges for the practical implementation of bacterial metabolic modelling computational tools in the pathogenesis field.

Once relegated to the supply of energy and biosynthetic precursors, it is now indubitable that metabolism mediates most of physiological processes. In the context of bacterial–host interactions where virulence is the outcome (commonly termed bacterial pathogenesis) metabolism expands far beyond its canonical role in bacterial proliferation. In addition to all sorts of recognized molecular determinants or virulence factors (toxins, flagella, translocated effectors, adhesins, invasins, etc.), bacterial pathogens are equipped with specific metabolic traits to circumvent immune defenses and antimicrobial killing, thus facilitating colonization and proliferation within their hosts. As the implementation of high‐throughput technologies elevates the pathogenesis field to the era of big data, it concurrently creates considerable challenges for our ability to interpret large data sets and identify factors that impact infectious processes. Metabolic modelling is emerging as a powerful tool allowing the integration and coherent organization of large data sets into the context of biological networks providing non‐intuitive insights on biological systems that experimental analysis alone cannot provide. Here, we take a snapshot of the recent understanding of bacterial metabolism and the bacterial–host metabolic interplay during infection, and highlight key outcomes and challenges for the practical implementation of bacterial metabolic modelling computational tools in the pathogenesis field (summarized in Fig. 1).Open in a separate windowFig. 1Genome‐scale metabolic network reconstructions for bacterial pathogenesis: it is time to leave a mark. Fast evolving advances in the genomics and metabolomics fields facilitate metabolic modelling of priority pathogens, of polymicrobial communities where key pathogens may have a starring role, and of host–pathogen systems. Metabolic reconstructions can yield significant benefits when combined with various layers of multi‐omics information as part of integration strategies, further enriched by the predictive potential of machine learning computational tools. Such integrative view will guide our experimental work to understand key metabolic traits in bacteria–bacteria or bacteria–host interactions where virulence is the outcome. More importantly, we foresee that such integrative view will contribute to pave the way for developing new diagnostic, treatment and surveillance procedures, seeking for their ultimate positive impact in the clinical management of bacterial infectious diseases.     

Effectiveness of three Glomus species in protecting pepper (Capsicum annuum L.) against verticillium wilt

The objective of this work was to study the influence of three Glomus species—Glomus mosseae (Nicol. and Gerd.) Gerd. and Trappe, Glomus intraradices (Schenck and Smith) and Glomus deserticola (Trappe, Bloss, and Menge)—on the development of Verticillium-induced wilt in Capsicum annuum cv. Piquillo. Results showed that the effectiveness of arbuscular mycorrhizal fungi (AMF) as biocontrol agents varied among different Glomus species. In pepper colonized by G. intraradices the severity of the disease was even higher than that observed in non-mycorrhizal plants in terms of plant growth and pepper yield. On the other hand, the high effectiveness exhibited by G. mosseae in improving plant growth and the early beginning of the reproductive stage in these plants was not associated with great plant protection and high pepper yield in diseased plants. Only plants associated with G. deserticola had greater yield than non-mycorrhizal ones despite the lower P fertilization applied to the mycorrhizal treatment and this fact was observed in both healthy and diseased plants. It is suggested that the higher specific phosphorus uptake in Verticillium-inoculated plants associated with G. deserticola could contribute to diminish the deleterious effect of pathogen on yield. On the other hand, the possible influence of endogenous phenolics in roots on the tolerance or resistance of pepper against wilt induced by Verticillium dahliae remains unclear.     

Nontypable Haemophilus influenzae displays a prevalent surface structure molecular pattern in clinical isolates

Non-typable Haemophilus influenzae (NTHi) is a gram negative pathogen that causes acute respiratory infections and is associated with the progression of chronic respiratory diseases. Previous studies have established the existence of a remarkable genetic variability among NTHi strains. In this study we show that, in spite of a high level of genetic heterogeneity, NTHi clinical isolates display a prevalent molecular feature, which could confer fitness during infectious processes. A total of 111 non-isogenic NTHi strains from an identical number of patients, isolated in two distinct geographical locations in the same period of time, were used to analyse nine genes encoding bacterial surface molecules, and revealed the existence of one highly prevalent molecular pattern (lgtF+, lic2A+, lic1D+, lic3A+, lic3B+, siaA-, lic2C+, ompP5+, oapA+) displayed by 94.6% of isolates. Such a genetic profile was associated with a higher bacterial resistance to serum mediated killing and enhanced adherence to human respiratory epithelial cells.     

Novel blaROB-1-Bearing Plasmid Conferring Resistance to β-Lactams in Haemophilus parasuis Isolates from Healthy Weaning Pigs

Haemophilus parasuis, the causative agent of Glässer''s disease, is one of the early colonizers of the nasal mucosa of piglets. It is prevalent in swine herds, and lesions associated with disease are fibrinous polyserositis and bronchopneumonia. Antibiotics are commonly used in disease control, and resistance to several antibiotics has been described in H. parasuis. Prediction of H. parasuis virulence is currently limited by our scarce understanding of its pathogenicity. Some genes have been associated with H. parasuis virulence, such as lsgB and group 1 vtaA, while biofilm growth has been associated with nonvirulent strains. In this study, 86 H. parasuis nasal isolates from farms that had not had a case of disease for more than 10 years were obtained by sampling piglets at weaning. Isolates were studied by enterobacterial repetitive intergenic consensus PCR and determination of the presence of lsgB and group 1 vtaA, biofilm formation, inflammatory cell response, and resistance to antibiotics. As part of the diversity encountered, a novel 2,661-bp plasmid, named pJMA-1, bearing the bla_ROB-1 β-lactamase was detected in eight colonizing strains. pJMA-1 was shown to share a backbone with other small plasmids described in the Pasteurellaceae, to be 100% stable, and to have a lower biological cost than the previously described plasmid pB1000. pJMA-1 was also found in nine H. parasuis nasal strains from a separate collection, but it was not detected in isolates from the lesions of animals with Glässer''s disease or in nontypeable Haemophilus influenzae isolates. Altogether, we show that commensal H. parasuis isolates represent a reservoir of β-lactam resistance genes which can be transferred to pathogens or other bacteria.     

Klebsiella pneumoniae outer membrane protein A is required to prevent the activation of airway epithelial cells

Outer membrane protein A (OmpA) is a class of proteins highly conserved among the Enterobacteriaceae family and throughout evolution. Klebsiella pneumoniae is a capsulated gram-negative pathogen. It is an important cause of community-acquired and nosocomial pneumonia. Evidence indicates that K. pneumoniae infections are characterized by a lack of an early inflammatory response. Data from our laboratory indicate that K. pneumoniae CPS helps to suppress the host inflammatory response. However, it is unknown whether K. pneumoniae employs additional factors to modulate host inflammatory responses. Here, we report that K. pneumoniae OmpA is important for immune evasion in vitro and in vivo. Infection of A549 and normal human bronchial cells with 52OmpA2, an ompA mutant, increased the levels of IL-8. 52145-Δwca(K2)ompA, which does not express CPS and ompA, induced the highest levels of IL-8. Both mutants could be complemented. In vivo, 52OmpA2 induced higher levels of tnfα, kc, and il6 than the wild type. ompA mutants activated NF-κB, and the phosphorylation of p38, p44/42, and JNK MAPKs and IL-8 induction was via NF-κB-dependent and p38- and p44/42-dependent pathways. 52OmpA2 engaged TLR2 and -4 to activate NF-κB, whereas 52145-Δwca(K2)ompA activated not only TLR2 and TLR4 but also NOD1. Finally, we demonstrate that the ompA mutant is attenuated in the pneumonia mouse model. The results of this study indicate that K. pneumoniae OmpA contributes to attenuate airway cell responses. This may facilitate pathogen survival in the hostile environment of the lung.     

Novel S-ribosylhomocysteine analogues as potential inhibitors of LuxS enzyme

Selective cross-coupling of the protected 6-fluoro-6-iodo-alpha-D-ribo-hex-5-enofuranose with 2 equivalents of 4-ethoxy-4-oxobutylzinc bromide in the presence of Pd[P(Ph)(3)](4) followed by deprotections gave methyl 5,6,7,8,9-pentadeoxy-6-fluoro-alpha/beta-D-ribo-dec-5(Z)-enofuranuronate; a S-ribosylhomocysteine analogue with the sulfur and carbon-5 atoms replaced by the fluoro(vinyl) unit.     

À la carte transcriptional regulators: unlocking responses of the prokaryotic enhancer-binding protein XylR to non-natural effectors

To investigate the activation mechanism of the enhancer-binding protein XylR encoded by the TOL plasmid of Pseudomonas putida mt-2, a combinatorial library was generated composed of shuffled N-terminal A domains of the homologous regulators DmpR, XylR and TbuT, reassembled within the XylR structure. When the library was screened in vivo for responsiveness to non-effectors bulkier than one aromatic ring (such as biphenyl) or bearing an entirely different distribution of electronegative groups (e.g. nitrotoluenes), protein variants were found that displayed an expanded inducer range including the new effectors. Although the phenotypes endowed with the corresponding changes were largely similar, the modifications involved different sites within the A domain. The positions of the mutations within a structural model of the A domain suggest that expansion of the inducer profile can be brought about not only by changes in the effector pocket of the protein but also by unlocking steps of the signal transmission mechanism that follows effector binding. These results provide a rationale for evolving in vitro regulators à la carte that are responsive to predetermined, natural or xenobiotic chemical species.