In earlier studies, phosphoglycerate kinase was reported on the s

In earlier studies, phosphoglycerate kinase was reported on the surface of S. pneumoniae, was antigenic in humans, and elicited protective immune responses in mouse model [33] [see Additional file 6]. Also in Schistosoma mansoni, phosphoglycerate kinase has been identified as a protective antigen [34]. Another surface protein, EF-G, identified in this study was found to be immuno-reactive against sera from broiler

chicken immune to necrotic entritis [30]. The protein was secreted into the culture supernatant and unique to virulent C. perfringens strain CP4 causing necrotic entritis. Notably, EF-G is regulated Selleck PF-6463922 by the VirR-VirS virulence regulon of C. perfringens [35]. Moreover, EF-G has been demonstrated as an immunogenic protein and was identified in both cell surface and extracellular fraction

of B. anthracis [9, 29]. Further, choloylglycine hydrolase family protein, cell wall-associated serine proteinase, and rhomboid family protein can be excellent surface protein markers for specific BAY 11-7082 in vitro detection of C. perfringens from environment and food as they share very low percent amino acid sequence identity with there nearest homologs (<50%) and are conserved among the C. perfringens strains [see Additional file 6]. Some of the surface proteins from C. perfringens ATCC13124 showed metabolic functions that would typically place them in the cytoplasm. Moreover, except for N-acetylmuramoyl-L-alanine amidase and cell wall-associated serine proteinase, these proteins have no N-terminal signal peptide and do not possess the canonical gram-positive anchor motif LPXTG [see Additional file 7]. Several surface-associated cytoplasmic proteins reported in this study were also detected on the bacterial surface in previous proteomic analysis [see Additional file 6]. For example, phosphoglycerate kinase was reported on the surface of S. pneumoniae [33], S. agalactiae [24], S. pyogenes [25], and S. oralis [see Additional file 6] and also as secreted protein in B. anthracis [29]. Increasing number of reports have shown presence of proteins on the surface of Gram positive bacteria or secreted into the medium that one would otherwise

expect to be cytoplasmic [25, 29, 36, 37]. In a previous study, the culture supernatant of C. perfringens at the late selleck compound exponential Cepharanthine growth phase was shown to contain intracellular proteins that had no putative signal sequences, such as ribokinase, β-hydroxybutyryl-coenzyme A dehydrogenase, fructosebisphosphate aldolase, and elongation factor G [36]. In other studies also, a significant number of cytoplasmic proteins have been identified as cell-wall associated proteins/immunogens [25, 37]. In spite of a growing list of cytoplasmic proteins identified on the bacterial surface, the mechanism of their surface localization and attachment to the bacterial envelope remain unclear. Internal signal sequences, posttranslational acylation, or an association with a secreted protein are hypothesized as possible means [38].

Results and discussion Time course of PHB granule formation in R

Results and discussion Time course of PHB granule formation in R. eutropha HF39 and H16 To study the formation and localization of PHB granules in R. eutropha we used R. eutropha MM-102 in vivo strains H16 and HF39. Both strains have wild type properties with respect to PHB metabolism Pictilisib research buy and easily form PHB granules during growth on rich media such as NB medium media. Strain HF39 is a spontaneous streptomycin resistant mutant of strain H16 and has often been used in place of strain H16 in conjugation experiments because of simplified counter selection of the donor [39]. In this study, the same results were obtained for both strains with the exception that strain HF39 grew slightly slower and produced in average

a lower number of PHB granules

than strain H16. Although R. eutropha strains H16 and HF39 intermediately accumulated PHB during growth on NB-medium more than 95% of the cells were free of PHB granules in the stationary growth phase after 24 h. Cells that still had PHB granules after this time period (<5%) often were division-inhibited (cells > 10 μm in length) and LY2874455 manufacturer many of them were dead as revealed by staining with propidium iodide (images not shown). In conclusion, most living cells of the late stationary growth phase of R. eutropha on NB-medium were free of accumulated PHB. To monitor the time course of PHB granule formation we transferred PHB-free stationary R. eutropha cells to fresh NB-medium that had been additionally supplemented with 0.2% sodium gluconate. This increased the C to N ratio of the medium and promoted PHB accumulation. Samples were taken at zero time and after 10 min to several hours

of growth. Harvested cells were chemically fixed, embedded in a low viscosity acrylic resin and subjected to thin section electron transmission microscopy. PHB granules poorly bind heavy atom stains and therefore have an electron-transparent (“white”) appearance. The results are as shown in Figures 1, 2, 3, 4, 5 and 6. Figure 1 TEM images of R. eutropha H16 (a) and of R. eutropha HF39 (b) after 24 h of growth on NB medium Tideglusib (=zero control [t=0 min after transfer to fresh NB-gluconate medium]). Cells were harvested, fixed and prepared for TEM as described in method section. All thin sections were stained with uranyl-acetate and lead citrate. Arrowheads indicate condensed cytoplasm resulting in an electron-transparent fringe between cytoplasm membrane and cytoplasm. Short arrows indicate the border between cytoplasm and denatured nucleoid. The long arrow in the left cell of (a) points to a small globular structure most likely representing an electron-transparent (“white”) remaining, not completely mobilised PHB granule. Note, the PHB granule is in close contact to nucleoid region. Bar represents 0.2 μm. Figure 2 Time course of PHB granule formation in R. eutropha H16 and HF39.

MH, ELH, MK and RJL wrote the manuscript MK and ELH contributed

MH, ELH, MK and RJL wrote the manuscript. MK and ELH contributed equally.”
“Background Salmonella is a gram-negative, facultative

anaerobic, flagellated bacterium. It is the pathogenic agent of salmonellosis, a major cause of enteric illness and typhoid fever, leading to many LY2228820 price hospitalisations and a few rare deaths if no antibiotics are administered. Salmonella outbreaks are linked to unhygienic food preparation, cooking, reheating and storage practices. The bacterium can be isolated from raw meat and poultry products as well as from milk and milk-based products [1]. The detection of Salmonella therefore remains a highly important issue in microbiological analysis for food safety and standards. Because the nomenclature for the Salmonella genus is at times confusing, this publication will follow the current literature [2, 3]. The CDC [3] distinguishes PXD101 in vitro two Salmonella species (or subgenera): S. enterica and S. bongori. S. enterica is further divided into six subspecies, of which S. enterica subsp. enterica is the most clinically significant, causing 99% of Salmonella infections. In the present study we are concerned with its two main serovars: Salmonella enterica serovar Typhimurium (group D) denoted S. Typhimurium, and Salmonella enterica serovar Enteritidis

(group B) denoted S. Enteritidis, which are the most commonly isolated Salmonellae from food-borne outbreaks. Identification of the disease-causing

Salmonella serovars is currently a lengthy process, and its initial isolation from food samples can SYN-117 be difficult as the bacteria can be present in small numbers and many closely related bacteria may be found within the same sample [4]. For this reason, pre-enrichment steps are required Succinyl-CoA for all samples [5, 6]. The current accepted method for isolation of Salmonella from foodstuffs is a well established procedure – ISO 6579, laborious and time-consuming, taking up to 5 days to complete [7, 8]. The most widely-used method used to characterise Salmonella into its subspecies is the Kauffman-White serotyping system [9], based on the variability of the O, H and Vi antigens [9–11]. Apart from being arduous, this method can not identify a small number of S. enterica samples that lack either the O antigen alone or both the O and the H antigens [12]. Therefore there is a need for fast, sensitive and specific “”in the field”" detection, using nucleic acid-based technologies such as molecular beacon-based real-time PCR, to reduce the time needed to complete the assay, but also improve the level of accuracy and reliability. In this study, molecular beacons [13–15] and real-time PCR technology are combined to develop a fast, sensitive, clear-cut method of detection of Salmonella spp.

We were curious whether intraperitoneal injections might be effec

We were curious whether intraperitoneal injections might be effective. Comparison of aged matched controls revealed no differences in the distributions of microsphere Elacridar nmr labelling following intravenous vs. intraperitoneal injections, although the intravenous approach generally led to more intense labelling. This finding indicates that greater numbers of fluorescently labelled latex microspheres reached and were phagocytosed

by Kupffer cells after IV injection as compared to IP injection. This result is not surprising in light of the requirement that with IP injections, Epigenetics inhibitor the microspheres would need to first cross both the mesothelial lining of the visceral peritoneum and then cross either an endothelial barrier to enter the blood stream or a more permeable endothelial barrier to join the lymph; these steps may well reduce click here availability of the microspheres in reaching the Kupffer cells of the liver sinusoids. However, the similarity in patterns of labelling give

support to the notion that intraperitoneal injection provides a valid approach for Kupffer cell labelling in younger pups. In support of this notion, we [24] found that peptide-containing liposomes target liver hepatocytes when administered either IV or IP in young postnatal mice. Further, a recent report [25] demonstrated that patterns of Evans Blue labelling were similar following IV and IP injections in mice. When comparing the F4/80 labelling to the microsphere distribution it is evident that the size of the microsphere is important for determining their distribution pattern. The larger (0.2 μm) microspheres appear to be taken up within the liver primarily by the F4/80 positive Kupffer cells, while the smaller

(0.02 μm) microspheres appear to be taken up not only by the Kupffer cells, but also by the CD-34 positive endothelial cells. Not all microspheres can be identified conclusively as being within specific cell types; some of the microspheres appear to be located extracellularly, Glutathione peroxidase perhaps adhering to the plasmalemma of either Kupffer or endothelial cells prior to being engulfed by those cells. Identifying Kupffer Cells The types of cells that comprise the mouse liver are similar to those that have been described in other mammalian species. The most prominent cell type is the parenchymal hepatocyte [[8–10, 21]]. Non-parenchymal cells include the phagocytic Kupffer cells [[1–3, 7, 12–17, 21]], labelled with the F4/80 antibody [21, 22], which in the adult mouse liver are approximately 35% of the number of hepatocytes, and also the Ito stellate cells [[26–30]], whose numbers are about 8-10% of the number of hepatocytes. As with any organ, endothelial cells form much of the lining of the sinusoidal capillaries.

It seems that actin cytoskeleton formation played a major role in

It seems that actin cytoskeleton formation played a major role in S. aureus internalization since cytochalasin D, an inhibitor that disrupts actin filament polymerization, selleck inhibitor led to up to 50% inhibition of S. aureus internalization. This finding was consistent with other studies [23,32] where actin filament was determined to play a dominant role in S. aureus internalization. One limitation of this study was that MOIs lower than 100:1 were not investigated and the higher MOI may only apply to infected tissues where numerous bacteria may exist. Future studies may need to consider lower MOIs. Note that our data confirmed that gentamicin treatment

was effective in eliminating extracellular S. aureus and the post-infection CFU was indeed from live intracellular S. aureus. Gentamicin treatment is commonly used to eliminate extracellular bacteria [21,32], but such a procedure lacks direct confirmation of live intracellular bacteria. In this study, besides culturing

the washing media collected after gentamicin treatment, the dual staining approach combined with confocal microscopy presented direct evidence that no live extracellular S. aureus was observed after the ACP-196 gentamicin treatment (Figure 3C). S. aureus has been thought to be a frequent cause for several types of chronic and recurrent infections including osteomyelitis, endovascular diseases, and chronic lung infections [33], and S.

aureus infections have been reported in clinical cases to persist asymptomatically with relapses occurring months or even years after apparent antimicrobial cure of the infections [34,35]. In these cases, S. aureus may have protected itself and escaped antibiotics and immune response of the host by “hiding” intracellularly and establishing a latent bacterial reservoir. This was supported by our observation that S. aureus could survive intracellularly for about up to 5 and 7 days, respectively, within macrophages and osteoblasts (Figure 2). As a phagocytic cell, macrophages were obviously more effective than osteoblasts at not only phagocytizing but also destroying the intracellular bacteria. This was supported by our data showing that S. aureus infection not only significantly increased the H2O2 levels in macrophages at 1 h infection but also significantly increased the O. 2 − levels in macrophages at infection times of 0.5 and 1 h. In contrast, S. aureus infection induced significantly higher levels of H2O2 in osteoblasts at 0.5 and 1 h infection but did not induce significant changes in O. 2 − levels in osteoblasts. As a result, a significantly higher number of intracellular CFUs was found in macrophages immediately after infection while significantly less intracellular S.

5 U aldolase, 0 5 U glycerolphosphate dehydrogenase and 0 5 U tri

5 U aldolase, 0.5 U glycerolphosphate dehydrogenase and 0.5 U triosephosphate isomerase. Metabolic flux selleck products calculations Metabolic flux calculations were performed as described previously [18]. Briefly, metabolic flux ratio analysis was used to gain information about the flux distribution at important branch points within the network. As several alternative pathways may lead to a particular product, the fractional contribution (metabolic flux ratio) of each pathway was determined based on the molecular Dibutyryl-cAMP mass distributions of the reactants and the

product according to Fischer and Sauer [33]. For the performed calculations, corrected mass spectra of selected fragments of serine, glycine, alanine, phenylalanine, tyrosine, aspartate and glutamate were used in this study (see Table 1). As the amino acids are synthesised from precursor metabolites of the central carbon metabolism with a known and well conserved carbon transition, their labelling pattern can be used to conclude the corresponding labelling pattern of their precursors [34]. To gain important information about the position of the labelling within the molecule, different fragments were considered simultaneously. PX-478 In general, TBDMS-derivatised amino acids yield characteristic fragments by electron impact ionisation. The [M-57] fragment of each amino acid contains the complete carbon backbone, whereas the

[M-85] fragment lacks the carbon at the C1 position Megestrol Acetate that corresponds to the carbon atom of the carboxyl group of the amino acid. The third fragment considered – [f302] – always contains the C1 and C2 carbon of the corresponding amino acid. In the case of alternative pathways yielding a specific product, the fractional contribution of each pathway can be determined

concerning the mass distributions of the reactants and the product according to Eq. (1) [33]. (1) In Eq. (1) index X indicates the product molecule whereas the consecutive numbers 1 through n represent reactant molecules of alternative pathways contributing to the mass distribution of the product pool. The corresponding fractional amount of each pathway f can then be calculated by considering two additional constraints: (i) all fractions must have a positive value and (ii) their sum has to equal 1. A more detailed description will be given in the following respective sections. Theoretical framework for flux estimation To carry out metabolic flux calculations for D. shibae and P. gallaeciensis, a metabolic network was constructed based on genome data (GenBank accession numbers NC_009952 [D. shibae] and NZ_ABIF00000000 [P. gallaeciensis]). As we focused on the central carbon metabolism, the major catabolic routes for glucose as well as the reactions linking the C3 and C4 pools were considered. In terms of glucose catabolism, the annotated genome revealed the presence of the genes encoding for glycolytic enzymes, enzymes of reactions in both the PPP and the ED pathway and TCA cycle. For D.

Pest Biochem Phys 101:39–47 Inada K (1976) Action spectra for pho

Pest Biochem Phys 101:39–47 Inada K (1976) Action spectra for photosynthesis in higher plants. Plant Cell Physiol 17:355–365 Ioannidis N, Schansker G, Barynin VV, Petrouleas V (2000) Interaction of nitric oxide with the oxygen evolving complex of photosystem II and manganese catalase: a comparative study. J Bioinorg Chem 5:354–363 Iwai M, Takahashi Y, Minagawa Y (2008) Molecular remodeling of photosystem II during state transitions in Chlamydomonas reinhardtii. Plant Cell 20:2177–2189PubMedCentralPubMed Jakob T, Goss R, Wilhelm C (1999) Activation of diadinoxanthin de-epoxidase due to a chlororespiratory proton gradient in the dark in the diatom Phaeodactylum

tricornutum. Plant Biol 1:76–82 Johnson

MP, Goral TK, Duffy CD, Brain AP, Mullineaux CW, Ruban AV (2011) Photoprotective energy dissipation involves the reorganization of photosystem II light-harvesting complexes in the grana membranes of spinach chloroplasts. HKI 272 Plant Cell 23:1468–1479PubMedCentralPubMed Joliot PA, Finazzi G (2010) Proton equilibration in the chloroplast modulates multiphasic kinetics of nonphotochemical quenching of fluorescence in plants. Proc Natl Acad Sci USA 107:12728–12733PubMedCentralPubMed Joly D, Carpentier R (2009) Sigmoidal reduction kinetics of the photosystem II acceptor side in intact photosynthetic materials during fluorescence induction. Photochem Photobiol Sci 8:167–173PubMed Kalaji MH (2011) The impact of abiotic stress factors on the fluorescence see more of chlorophyll in CB-839 mouse plants of selected varieties of barley (Hordeum vulgare L.). Warsaw University of Life Sciences SSGW, Warsaw, (in Polish) Kalaji MH, Guo P (2008) Chlorophyll fluorescence: a useful tool in barley plant breeding programs. In: Sanchez A, Guttierez SJ (eds) Photochemistry research in progress. Nova, New York, pp 439–463 Kalaji MH, Loboda T (2010) Chlorophyll fluorescence to study of the physiological status of plants. Warsaw Agricultural University, Warsaw, p 116 Kalaji MH, Bosa K, Koscielniak J, Hossain Z (2011a) Chlorophyll a fluorescence—a useful tool for the early detection of temperature stress in spring barley (Hordeum vulgare L.).

OMICS J Integr Biol 15:925–934 Kalaji MH, Govindjee, Bosa K, Kościelniak IKBKE J, Żuk-Gołaszewska K (2011b) Effects of salt stress on photosystem II efficiency and CO2 assimilation of two Syrian barley landraces. Environ Exp Bot 73:64–72 Kalaji MH, Carpentier R, Allakhverdiev SI, Bosa K (2012a) Fluorescence parameters as an early indicator of light stress in barley. J Photochem Photobiol B 112:1–6PubMed Kalaji MH, Goltsev V, Bosa K, Allakhverdiev SI, Strasser RJ, Govindjee (2012b) Experimental in vivo measurements of light emission in plants: a perspective dedicated to David Walker. Photosynth Res 114:69–96PubMed Kasahara M, Kagawa T, Oikawa K, Suetsuga N, Miyao M, Wada M (2002) Chloroplast avoidance movement reduces photodamage in plants.

Authors’ contributions Experiments were designed by CJL and MMY a

Authors’ contributions Experiments were designed by CJL and MMY and performed by MMY, ZYW, and WW. Results were analyzed and interpreted by MMY, ZYW, and WW. The manuscript was written by MMY and CJL. CJL is in charge of the project direction, planning, and organization. All authors read and approved the final manuscript.”
“Background Self-assembled metallic droplets

have been attracting considerable attention due to their outstanding physical and optoelectronic properties such as an improved optical absorption at their localized surface plasmon resonance (LSPR) frequency, the shift of wavelengths and the local heating, etc. through the interactions with quantum and nanostructures and thus have found various applications with diverse semiconductors. For Dorsomorphin selleck compound example, self-assembled droplets can act as a nanoscale surface drilling medium for the fabrication of ‘nanoholes’ using the droplet etching technique [1–4]. Quantum dots have then been demonstrated around the nanoholes [5]. Also, metallic droplets have been successfully utilized in the fabrications of various quantum- and nanostructures such as quantum rings [6–9], quantum dots [10–12], and nanowires (NWs) [13] through ‘droplet epitaxy’ following the successful fabrication of homo-epitaxial GaAs nanocrystals on a GaAs substrate [14]. In addition, Au droplets have been adapted

as catalysts for the fabrication of diverse NWs via various epitaxial approaches and have attracted extensive interest due to their unique properties such as surface plasmonic resonance, biosensing, quantum size effect, and biology [15–18]. Moreover, given the wide range of substrates and vapor SPTLC1 phase materials utilized, Au droplets can be successfully utilized in the fabrication of various NWs and many elements utilized can diffuse into catalyst gold droplets based on the vapor-liquid-solid (VLS) mechanism during the fabrication of NWs [19–27]. For example, Si, Ge, GaN, GaAs, and InAs-InSb NWs have been successfully synthesized by molecular beam epitaxy, chemical beam epitaxy, pulsed laser deposition, and chemical vapor deposition

[28–30]. In the VLS-based growth, from the supersaturated catalyst alloy droplets, the nucleation and growth of NWs can occur at the L-S interface due to a much higher sticking probability. Therefore, the design of NWs including diameter, length, configuration, and density is originally determined by that of the Au droplet catalysts. Consequently, the study of the behavior of Au droplets on various surfaces becomes an essential step to accomplish desired NW synthesis; however, to date, the systematic study of the control of Au droplets on GaAs is still deficient. Therefore, in this study, we investigate the effect of systematic thickness variation on self-assembled Au droplets on GaAs (111)A and (100). Methods In this study, the fabrication of Au droplets was carried out on GaAs (111)A and semi-insulting (100) substrates in a pulsed laser deposition (PLD) system.

Interestingly, infection of Huh-7 cells with such particles led u

Interestingly, infection of Huh-7 cells with such particles led us to isolate cellular clones exhibiting different levels of permissivity to HCVcc and HCVpp. For most of them, reduced HCV infection levels were directly related to their reduced expression level of CD81, while

other entry molecules such as SR-BI and CLDN-1 were not modified. Our observation is in accordance with previously published data [29, 48–50]. Ectopic expression of CD81 in Huh-7w7 cells, one of the resistant cell clones, restored HCV permissivity indicating that CD81 deficiency alone was responsible for the resistance to HCV infection in these cells. In agreement with previous studies [29, 48, 51], we did not observe any variation in HCV genome replication in Huh-7w7 AICAR cells in comparison to Huh-7 cells (data not shown), suggesting that CD81 is not involved in this step of the viral cycle. Masciopinto et al. showed that CD81 and HCV envelope glycoproteins could be detected in exosomes of mammalian cells,

suggesting that HCV may intracellularly interact with CD81 allowing its export [52]. They pointed out a possible role of CD81 selleck compound in assembly and release of HCV particles. However, our results indicate that CD81 does not participate to HCV assembly or release of new viral particles, since the supernatant of Huh-7w7 cells transfected with full-length HCV RNA infected naïve Huh-7 cells to a level comparable to that of the supernatant from transfected Huh-7 cells. Thus, Huh-7w7 cells constitute a new tool allowing to investigate the involvement of CD81 in HCV entry and offering a new single-cycle replication system, as already used by others [29]. The molecular determinants of HCV-CD81

interaction have been analyzed by several groups by using biochemical assays (reviewed in [53]). However, Flint et al have highlighted the limitation of these AZD6094 molecular weight approaches Levetiracetam since various mutated CD81 sequences previously reported to abrogate E2-CD81 interaction, were able to restore permissivity in HepG2 cells [15]. In our study, we show that ectopic expression of human and mouse CD81 proteins in human hepatoma cells devoid of CD81 conferred susceptibility to infection by HCVcc and HCVpp at various levels. Interestingly, mCD81 protein supports infection by HCVcc and HCVpp bearing glycoproteins from genotypes 2a and 4 suggesting that, in accordance with other studies [15, 17], CD81 is not the sole determinant of species susceptibility to HCV. Other additional cellular factors likely modulate HCV entry. In addition, interaction/organization levels and stoichiometry between entry factors and plasma membrane lipids may regulate species susceptibility to HCV. CD81 belongs to the tetraspanin family of which members have the distinctive feature of clustering dynamically with numerous partner proteins and with one another in membrane microdomains.

None of the tested isolates grown in ASM (from both treatment and

None of the tested isolates grown in ASM (from both treatment and control groups) displayed the hypermutable phenotype. The only hypermutable isolate detected in this study was generated following growth in Luria Bertani (LB) for 18 hours (Figure 2 Pevonedistat purchase and Table 1). Although diversification occurred with respect to only a few of the phenotypic properties tested, the proportions of the isolates exhibiting these traits varied considerably

between treatment groups (Figure 1). The proportions of these phenotypic changes accounted for the within and between-treatment group variation seen in the numbers of mutant haplotypes (Figure 1). Hierarchical analysis of variance indicated that the majority (77%) of diversity was distributed between isolates within populations, rather than the same traits systematically apportioned between replicate populations or between treatments (Table 2). Table 2 Hierarchical analysis of variance (σ 2 ) for diversity   Sigma % Variations between treatment 0.03 6.18 Variations between samples within treatment 0.09 16.42 Variations within samples 0.42 77.40 Total Olaparib cost variations 0.54 100.00 INCB018424 Discussion Although it is known that the phenotypic and genotypic characteristics of

P. aeruginosa populations within the CF lung fluctuate over time [9, 16], the factors that are responsible for this diversification are not fully understood. When P. aeruginosa LESB58 was grown in ASM with and without sub-inhibitory concentrations of antibiotics, we observed differential effects of antibiotics commonly used to treat CF patients on the diversity of LESB58 populations in the ASM model. In particular, increased levels of phenotypic diversification occurred in LESB58 populations grown in ASM when sub-inhibitory concentrations of colistin, ceftazidime and azithromycin were present. However, extensive

diversification of the P. aeruginosa populations was not seen in the presence of sub-inhibitory concentrations of meropenem. There are a number of mechanisms by which sub-inhibitory concentrations of antibiotics could potentially enhance bacterial diversification. One potential mechanism could involve the antibiotics inducing mutagenesis within bacterial populations, causing variation and/or promoting the hypermutability phenotype [31–34]. A second potential HSP90 mechanism could involve the antibiotics acting as signalling molecules, altering the QS systems within bacterial populations and subsequently promoting social evolution and diversification [35, 36, 38]. Antibiotic exposure has been shown to induce mutagenesis by triggering the SOS response and thus increasing the expression of error-prone DNA polymerases, which could give rise to diversity within bacterial populations [31–34]. It is possible that ceftazidime induced mutagenesis in the LESB58 populations through the induction of the SOS response.