Notes

Downstream of GA4, PbCYP78A6 participates in regulatory cellular cycle-related body's genes and also parthenogenesis in pear (Pyrus bretshneideri Rehd.).
In contrast, Fur activates the transcription of vieSAB in a direct manner. The cdgD and vieSAB encode proteins with GGDEF and EAL domains, respectively. Thus, data presented here highlight a new physiological role for Fur wherein it acts as a repressor of V. cholerae biofilm formation mediated by decreasing the production of exopolysaccharide and the intracellular levels of c-di-GMP.A nitrate- and metal-contaminated site at the Oak Ridge Reservation (ORR) was previously shown to contain the metal molybdenum (Mo) at picomolar concentrations. This potentially limits microbial nitrate reduction, as Mo is required by the enzyme nitrate reductase, which catalyzes the first step of nitrate removal. Enrichment for anaerobic nitrate-reducing microbes from contaminated sediment at the ORR yielded Bacillus strain EB106-08-02-XG196. This bacterium grows in the presence of multiple metals (Cd, Ni, Cu, Co, Mn, and U) but also exhibits better growth compared to control strains, including Pseudomonas fluorescens N2E2 isolated from a pristine ORR environment under low molybdate concentrations ( less then 1 nM). Molybdate is taken up by the molybdate binding protein, ModA, of the molybdate ATP-binding cassette transporter. ModA of XG196 is phylogenetically distinct from those of other characterized ModA proteins. The genes encoding ModA from XG196, P. fluorescens N2E2 and Escherichia coli K12 were expressed in E. coli and the recombinant proteins were purified. Isothermal titration calorimetry analysis showed that XG196 ModA has a higher affinity for molybdate than other ModA proteins with a molybdate binding constant (K D ) of 2.2 nM, about one order of magnitude lower than those of P. fluorescens N2E2 (27.0 nM) and E. coli K12 (25.0 nM). XG196 ModA also showed a fivefold higher affinity for molybdate than for tungstate (11 nM), whereas the ModA proteins from P. fluorescens N2E2 [K D (Mo) 27.0 nM, K D (W) 26.7 nM] and E. coli K12[(K D (Mo) 25.0 nM, K D (W) 23.8 nM] had similar affinities for the two oxyanions. We propose that high molybdate affinity coupled with resistance to multiple metals gives strain XG196 a competitive advantage in Mo-limited environments contaminated with high concentrations of metals and nitrate, as found at ORR.[This corrects the article DOI 10.3389/fmicb.2019.01434.].Histomonosis in chickens often appears together with colibacillosis in the field. Thus, we have experimentally investigated consequences of the co-infection of birds with Histomonas meleagridis and avian pathogenic Escherichia coli (APEC) on the pathology, host microbiota and bacterial translocation from the gut. Commercial chicken layers were infected via oral and cloacal routes with lux-tagged APEC with or without H. meleagridis whereas negative controls were left uninfected. Except one bird, which died due to colibacillosis, no clinical signs were recorded in birds infected with bioluminescence lux gene tagged E. coli. In co-infected birds, depression and ruffled feathers were observed in 4 birds and average body weight gain significantly decreased. Typhlitis caused by H. meleagridis was present only in co-infected birds, which also had pronounced microscopic lesions in systemic organs such as liver, heart and spleen. The 16S rRNA gene amplicon sequencing showed that in co-infected birds, corresponding to as avian pathogenic E. coli in the gut and increased penetration of E. coli from the cecal lumen toward peritoneum. This study provides novel insights into the parasite-bacteria interaction in vivo highlighting the role of H. meleagridis to support E. coli in the pathogenesis of colibacillosis in chickens.Tenacibaculosis remains a major health issue for a number of important aquaculture species globally. On the west coast of Canada, yellow mouth (YM) disease is responsible for significant economic loss to the Atlantic salmon industry. While Tenacibaculum maritimum is considered to be the primary agent of clinical YM, the impact of YM on the resident microbial community and their influence on the oral cavity is poorly understood. Using a 16s rRNA amplicon sequencing analysis, the present study demonstrates a significant dysbiosis and a reduction in diversity of the microbial community in the YM affected Atlantic salmon. The microbial community of YM affected fish was dominated by two amplicon sequence variants (ASVs) of T. maritimum, although other less abundant ASVs were also found. Interestingly clinically unaffected (healthy) and YM surviving fish also had a high relative abundance of T. maritimum, suggesting that the presence of T. maritimum is not solely responsible for YM. A statistically significant association was observed between the abundance of T. maritimum and increased abundance of Vibrio spp. within fish displaying clinical signs of YM. Findings from our study provide further evidence that YM is a complex multifactorial disease, characterized by a profound dysbiosis of the microbial community which is dominated by distinct ASVs of T. maritimum. Navarixin mw Opportunistic taxa, including Vibrio spp., may also play a role in clinical disease progression.Mycobacterium tuberculosis, the etiologic agent of human tuberculosis, is the world's leading cause of death from an infectious disease. One of the main features of this pathogen is the complex and dynamic lipid composition of the cell envelope, which adapts to the variable host environment and defines the fate of infection by actively interacting with and modulating immune responses. However, while much has been learned about the enzymes of the numerous lipid pathways, little knowledge is available regarding the proteins and metabolic signals regulating lipid metabolism during M. tuberculosis infection. In this work, we constructed and characterized a FasR-deficient mutant in M. tuberculosis and demonstrated that FasR positively regulates fas and acpS expression. Lipidomic analysis of the wild type and mutant strains revealed complete rearrangement of most lipid components of the cell envelope, with phospholipids, mycolic acids, sulfolipids, and phthiocerol dimycocerosates relative abundance severely altered.
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