,DNA sequences of each allele for 165 loci found in a population of 147 fully sequenced IncI2 plasmids with allelic identifiers.,Data is based on whole-genome sequences in the National Center for Biotechnology Information database as of July, 2017.,Resources in this dataset:,,

Background Local infection with necrotizing pathogens induces whole plant immunity to secondary challenge. Pathogenesis-related genes are induced in parallel with this systemic acquired resistance response and thought to be co-regulated. The hypothesis of co-regulation has been challenged by induction of Arabidopsis PR-1 but not systemic acquired resistance in npr1 mutant plants responding to Pseudomonas syringae carrying the avirulence gene avrRpt2. However, experiments with ndr1 mutant plants have revealed major differences between avirulence genes. The ndr1-1 mutation prevents hypersensitive cell death, systemic acquired resistance and PR-1 induction elicited by bacteria carrying avrRpt2. This mutation does not prevent these responses to bacteria carrying avrB. Results Systemic acquired resistance, PR-1 induction and PR-5 induction were assessed in comparisons of npr1-2 and ndr1-1 mutant plants, double mutant plants, and wild-type plants. Systemic acquired resistance was displayed by all four plant lines in response to Pseudomonas syringae bacteria carrying avrB. PR-1 induction was partially impaired by either single mutation in response to either bacterial strain, but only fully impaired in the double mutant in response to avrRpt2. PR-5 induction was not fully impaired in any of the mutants in response to either avirulence gene. Conclusion Two pathways act additively, rather than in an obligatorily synergistic fashion, to induce systemic acquired resistance, PR-1 and PR-5. One of these pathways is NPR1-independent and depends on signals associated with hypersensitive cell death. The other pathway is dependent on salicylic acid accumulation and acts through NPR1. At least two other pathways also contribute additively to PR-5 induction.

Background The gene encoding the inorganic pyrophosphatase (PPase) of the intracellular pathogen Legionella pneumophila is induced during intracellular infection, but is constitutively expressed in Eschericia coli. The causative agent of tuberculosis, Mycobacterium tuberculosis, contains a well conserved copy of PPase. We sought to determine if expression of the M. tuberculosis PPase is regulated by the intracellular environment. Results A strain of Mycobacterium bovis bacille Calmette-Guérin (BCG) was constructed in which the Aequoria victoria green fluorescent protein (GFP) is controlled by the promoter of the M. tuberculosis ppa gene. After prolonged exposure of the recombinant BCG strain within murine bone-marrow-derived macrophages, there was no observed increased activity of the ppa promoter. Furthermore, there was no change in promoter activity after exposure to various stress stimuli such as reduced pH, osmotic shock, nutrient limitation or oxidative stress. Conclusions These results suggest that macrophage induction of ppa is not a general phenomenon among intracellular pathogens.

Background Laboratory experiments under controlled conditions during thousands of generations are useful tools to assess the processes underlying bacterial evolution. As a result of these experiments, the way in which the traits change in time is obtained. Under these conditions, the bacteria E. coli shows a parallel increase in cell volume and fitness. Results To explain this pattern it is required to consider organismic and population contributions. For this purpose we incorporate relevant information concerning bacterial structure, composition and transformations in a minimal modular model. In the short time scale, the model reproduces the physiological responses of the traits to changes in nutrient concentration. The decay of unused catabolic functions, found experimentally, is introduced in the model using simple population genetics. The resulting curves representing the evolution of volume and fitness in time are in good agreement with those obtained experimentally. Conclusions This study draws attention on physiology when studying evolution. Moreover, minimal modular models appear to be an adequate strategy to unite these barely related disciplines of biology.

Selected bacterial, and antibiotic resistance genes sul and INTI1 concentrations by qPCR assays, and ASV tables of bacterial communities growing in biofilms incubated in river -and wastewater treatment plant effluent amended -river water. This dataset is associated with the following publication: Eytcheson, S., S. Brown, H. Wu, C. Nietch, P. Weaver, J. Darling, E. Pilgrim, T. Purucker, and M. Molina. Assessment of Emerging Pathogens and Antibiotic Resistance Genes in the Biofilm of Microplastics Incubated Under a Wastewater Discharge Simulation. Environmental Microbiology. Wiley-Blackwell Publishing, Hoboken, NJ, USA, 27(5): e70103, (2025).

Microorganisms' natural ability to live as organized multicellular communities – also known as biofilms – provides them with unique survival advantages. For instance, biofilms are protected against environmental stresses thanks to their extracellular matrix, which could contribute to persistent infections after treatment. Biofilms are also capable of strongly attaching to surfaces, where their metabolism byproducts could lead to surface material degradation. Furthermore, microgravity can alter biofilm behavior in unexpected ways, making the presence of biofilms in space a risk for both astronauts and spaceflight hardware. Despite the efforts to eliminate microorganism contamination from spacecrafts surfaces, it is impossible to prevent human-associated bacteria or fungus from eventually establishing biofilm surface colonization. Nevertheless, by understanding the changes that biofilms undergo in microgravity, it is possible to identify key differences and pathways that could be targeted to significantly reduce biofilm formation. The Space Biofilms project, performed at the International Space Station, contributes to such understanding by characterizing the morphology and gene expression of bacterial and fungal biofilms formed in microgravity with respect to ground controls. Pseudomonas aeruginosa was used as model organism for the bacterial morphology and transcriptomic studies, while Penicillium rubens was used for the fungal morphology study. Bacterial biofilm formation was characterized at one, two, and three days of incubation (37°C) over six different materials: stainless steel 316, passivated stainless steel 316, a lubricant impregnated surface (LIS), catheter grade silicone with and without a linear microtopography, and cellulose membrane.

,The biological materials in this section are unpatented, proprietary intellectual property, available for licensing under a Biological Materials License Agreement: Hybridoma Cell Lines; Microbial Isolates; Cloned Genetic Material; Cell Lines; Viruses; Plasmids. Updated June 2018.,,

Background Infections of bacterial cultures by bacteriophages are serious problems in biotechnological laboratories. Apart from such infections, prophage induction in the host cells may also be dangerous. Escherichia coli is a commonly used host in biotechnological production, and many laboratory strains of this bacterium harbour lambdoid prophages. These prophages may be induced under certain conditions leading to phage lytic development. This is fatal for further cultivations as relatively low, though still significant, numbers of phages may be overlooked. Thus, subsequent cultures of non-lysogenic strains may be infected and destroyed by such phage. Results Here we report that slow growth of bacteria decreases deleterious effects of spontaneous lambdoid prophage induction. Moreover, replacement of glucose with glycerol in a medium stimulates lysogenic development of the phage after infection of E. coli cells. A plasmid was constructed overexpressing the phage 434 cI gene, coding for the repressor of phage promoters which are necessary for lytic development. Overproduction of the cI repressor abolished spontaneous induction of the λimm434 prophage. Conclusions Simple procedures that alleviate problems with spontaneous induction of lambdoid prophage and subsequent infection of E. coli strains by these phages are described. Low bacterial growth rate, replacement of glucose with glycerol in a medium and overproduction of the cI repressor minimise the risk of prophage induction during cultivation of lysogenic bacteria and subsequent infection of other bacterial strains.

Background Many eukaryotes, including plants and fungi make spores that resist severe environmental stress. The micro-organism Dictyostelium contains a single phospholipase C gene (PLC); deletion of the gene has no effect on growth, cell movement and differentiation. In this report we show that PLC is essential to sense the environment of food-activated spores. Results Plc-null spores germinate at alkaline pH, reduced temperature or increased osmolarity, conditions at which the emerging amoebae can not grow. In contrast, food-activated wild-type spores return to dormancy till conditions in the environment allow growth. The analysis of inositol 1,4,5-trisphosphate (IP3) levels and the effect of added IP3 uncover an unexpected mechanism how PLC regulates spore germination: i) deletion of PLC induces the enhanced activity of an IP5 phosphatase leading to high IP3 levels in plc-null cells; ii) in wild-type spores unfavourable conditions inhibit PLC leading to a reduction of IP3 levels; addition of exogenous IP3 to wild-type spores induces germination at unfavourable conditions; iii) in plc-null spores IP3 levels remain high, also at unfavourable environmental conditions. Conclusions The results imply that environmental conditions regulate PLC activity and that IP3 induces spore germination; the uncontrolled germination of plc-null spores is not due to a lack of PLC activity but to the constitutive activation of an alternative IP3-forming pathway.