As expected, in Atg5−/− MEFs, LC3-II was never detected

whatever the cell culture conditions because the presence of Atg5 is absolutely required for the LC3 recruitment onto autophagosome membrane [19]. In WT MEFs infected with B. abortus or with B. melitensis, the relative abundance of LC3-I and LC3-II at 18 h p.i. did not change when compared to non-infected MEFs (Figure 1B). Figure 1 Relative abundance of LC3B-I and LC3B-II in WT MEFs and in Atg5 click here −/− MEFs as determined by immunoblotting. A. Cells were maintained in DMEM/FCS (F), starved for 2 h in EBSS (S) or incubated for 5 h in the presence of 100 nM bafilomycin (Baf). B. Cells were infected with B. abortus (BA) or with B. melitensis (BM) for 18 h or left non infected (Ctl). Replication of B. abortus- and B. melitensis-mCherry in Atg5−/− fibroblasts We studied the contribution of the macroautophagic pathway on the replication of Brucellae using Atg5-deficient MEFs. First, we infected cells with B. abortus-mCherry (Figure 2A) or with B. melitensis-mCherry

(Figure 2B) for 1 h at a multiplicity of infection (MOI) of 300. After inoculation, the medium was removed and replaced by a medium containing gentamicin to kill extracellular bacteria. selleck kinase inhibitor As it can be seen on micrographs taken after increasing times postinfection, B. abortus-mCherry is able to enter, survive and replicate in MEFs, even in Atg5-deficient MEFs. In both cell lines, at 6 h p.i, there are only a few bacteria per infected cell but this number massively increases between 12 and 18 h p.i. and at 24 h p.i., the bacteria are so abundant that it is difficult to enumerate them. B. melitensis-mCherry is also able to replicate in both WT MEFs and Atg5−/− MEFs. However, it is clear that www.selleck.co.jp/products/cobimetinib-gdc-0973-rg7420.html the number of bacteria per infected cell at 24 h p.i. is lower compared to B. abortus-mCherry. Statistical analysis of these observations revealed that there is no significant difference in the number of B. abortus-mCherry per infected cell between the Atg5-deficient MEFs and the WT MEFs whatever the time postinfection (Figure 3A). In contrast, the number of B. melitensis-mCherry

per infected cell significantly increased in Atg5−/− MEFs when compared to WT MEFs at 9 h, 18 h and 24 h p.i. (Figure 3B). These data demonstrate that both Brucella strains can survive and replicate when the conventional Atg5-dependent macroautophagic pathway is impaired. Atg5-deficient cells seem to be even more permissive for B. melitensis replication than WT MEFs. Figure 2 Fluorescence microscopy analysis of WT MEFs and Atg5 −/− MEFs infected with B. abortus -mCherry (A) or with B. melitensis- mCherry (B). MEFs were infected for 1 h with Brucella-mCherry at an MOI of 300 and observed at 6 h, 12 h, 18 h and 24 h p.i. The nuclei were stained with DAPI. Figure 3 Quantification of the infection of WT MEFs and Atg5 −/− MEFs with B. abortus -mCherry (A) or with B. melitensis- mCherry (B). MEFs were infected for 1 h with Brucella-mCherry at an MOI of 300.

Group-I included 15 strains that did not enter cells, formed no plaques and had no phospholipase activity. Group-II consisted of only one strain entering cells, forming no plaques and only expressing PI-PLC activity. Group-III comprised nine

strains entering cells, forming no plaques and only expressing PC-PLC activity. In this new analysis, the previously described Group-IV [7] has now been divided into 3 sub-Groups. The new Group-IV included nine strains forming plaques but fewer than virulent strains (mean 3 log versus 5). Three out of 9 strains were also characterized by a very low level of PC- and PI-PLC. The new Group-V comprised six strains also forming plaques but fewer than virulent strains ALK inhibitor and characterized by their very high PI-PLC activity. Finally, Group-VI contained three strains forming plaques within Sunitinib 48 h. In contrast the other strains formed plaques within 24 h, classic time necessary

to count the plaque number. Genotypic characterisation of the low-virulence strains Sequencing the prfA, plcA, plcB, inlA and inlB genes allowed us to observe that some phenotypes correlate with genotypic mutations which have been demonstrated to be the cause of the low virulence (Table 1) [7]. The sequences of the PrfA, InlA and ActA fragment were compared to those of the EGDe strain (serotype 1/2 – GenBank accession number AL591824) or F2365 strain (serotype 4 – GenBank accession number AE017262), according to the serotypes of the

strains. The phenotypic Group-I strains exhibited mutations in PrfA compared to the EGDe strain and were subdivised into 2 genotypic Groups: the PrfAK220T (genotypic Group-Ia) and the truncated PrfAΔ174-237 (genotypic below Group-Ib) previously described [8, 11]. One strain (NP26) exhibited a new putative causal mutation in prfA, K130Q, and is the only one of serotype 4b exhibiting a PrfA mutation (herein defined as genotypic Group-Ic). Two genotypic Groups were also identified for the phenotypic Group-III strains. One harbored exactly the same mutations in the plcA, inlA and inlB genes, characteristic of the previously genotypic Group-IIIa [8]. Only one strain (AF105) belonged to Group-IIIb and harbored a mutation at least in the inlA gene. No genotyping Group has been defined for the phenotypic Groups-II because this Group is formed by only one strain. The Group-IV, -V and –VI strains did not exhibit specific DNA sequence of the prfA, inlA and actA fragment genes, that allowed us to assign genotyping Groups. No causal mutations could have been displayed explaining the low virulence of these Groups. PFGE profiles To study the genetic relationships between the low-virulence strains, the 43 low-virulence strains were compared with 49 virulent strains (based on both the mouse s.c.

In: Mok DWS, Mok MC (eds) Cytokinins: chemistry, activity and function. CRC Press, Boca Raton, pp 179–195 Sathish P, Withana N, Biswas M, Bryant C, Templeton K, Al-Wahb M, Smith-Espinoza C, Roche JR, Elborough KM, Phillips JR (2007)

Transcriptome analysis reveals season-specific rbcS gene expression profiles in diploid perennial ryegrass (Lolium perenne L.). Plant Biotechnol J 5(1):146–161CrossRefPubMed ATM/ATR cancer Schmulling T, Schäfer S, Romanov G (1997) Cytokinins as regulators of gene expression. Physiol Plant 100:505–519CrossRef Soitama AJ, Piippo M, Allahverdiyea Y, Battchikova N, Aro EM (2008) Light has a specific role in modulating Arabidopsis gene expression at low temperature. BMC Plant Biol 8(1):13CrossRef Surpin M, Larkin RM, Chory J (2002) Signal transduction between the chloroplast and the nucleus. Plant Cell 14:S327–S328PubMed Synková H, Van Loven K, Pospišilová J, Valcke R (1999) Photosynthesis of transgenic Pssu-ipt tobacco. J Plant Physiol 155:173–182 Synková H, Pechova R, Valcke R (2003) Changes in chloropast ultrastructure

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Haplotype properties differ between different antibiotic exposures Diversification of P. aeruginosa LESB58 in ASM cultured with and without the various antibiotics was observed only with respect to colony morphology, pyocyanin production and antibiotic susceptibilities (Table 1). The culture of LESB58 in ASM with sub-inhibitory concentrations of ceftazidime

and colistin led to diversity in antimicrobial susceptibilities, changes in colony morphology and a loss of pyocyanin production (Table 1). LESB58 cultured in the presence of these antibiotics, generated more isolates that were outside the normal range of the antibiotic sensitivity profiles of LESB58 controls (Figure 3). In addition, exposure to azithromycin and tobramycin promoted increased cross-resistance Selleck Saracatinib to other antibiotics (Table 1, Figure 3). There

was no variation in the auxotrophic phenotype in the isolates analysed in all experimental and control groups (LESB58 has an auxotrophic phenotype). The populations exposed to meropenem exhibited no clear phenotypic diversification (Table 1 and Figure 2). Figure 3 Variations in zones of inhibition within LESB58 populations. The 120 LESB58 isolates obtained from the triplicate ASM cultures were assessed for susceptibility to six commonly used antibiotics (ceftazidime, ciprofloxacin, click here colistin, meropenem, tazobactam/piperacillin and tobramycin). Boxplots showing the range in the diameter of the zones of inhibition to these antibiotics are presented. 1. LB (18 hours) 2. ASM 3. ASM with ceftazidime 4. ASM with colistin 5. ASM with meropenem 6. ASM with tobramycin 7. ASM with azithromycin 8. Normal range of LESB58 (Groups 1–8: n = 120). The red line represents the cut-off for the the sensitivity of P. aeruginosa to the antibiotics tested, in accordance with the guidelines of Andrews

and Howe [37]. The values above the red line denote a higher sensitivity to antibiotics and the values below the line denote a higher resistance. Table 1 Number of isolates in each group (total of 120) exhibiting each of the traits measured   Colony morphology Virulence Mutations Outside normal range of antimicrobials susceptibility Culture Green non-mucoid Straw non-mucoid Pyocyanin Hypermutability Ceftazidime Ciprofloxacin Tobramycin Meropenem Colistin Tazobactam/piperacillin ASM 120 0 117 0 3 0 19 0 2 8 ASM + CAZ 110 10 92 0 16 19 20 18 10 11 ASM + CT 113 7 84 0 17 37 29 15 7 9 ASM + AZT 120 0 120 0 0 16 34 0 4 4 ASM + MEM 120 0 118 0 1 8 4 0 0 1 ASM + TOBI 118 2 119 0 1 24 69 3 22 1 LB (18 hours) 120 0 120 1 0 0 0 0 0 0 Isolates that were characterized as being outside the normal range of antimicrobial susceptibility typically observed in LESB58, included isolates that had either an increased or reduced susceptibility to the antibiotic under test. ASM = Artificial Sputum Medium, LB = Luria Bertani, CAZ = Ceftazidime, CT = Colistin, AZT = Azithromycin, MEM = Meropenem and TOBI = Tobramycin.

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Enteritidis PT4 P125109 chromosome and predicted as absent in the test strain. In red, genes absent in the S. Enteritidis PT4 P125109 chromosome and predicted as present in the test strain. In white, genes present or absent in both reference and test strains. Only those isolates for which any divergence is predicted are shown. S. Enteritidis PT4 P125109 results are shown as C646 molecular weight reference.

Detailed analysis of the genes within the DG showed that prophage-like elements constitute the major source of genetic variation distinguishing these S. Enteritidis isolates. However, this analysis also revealed some interesting differences in metabolic potential and in genes associated with restriction-modification systems (discussed below). S. Enteritidis variable prophage-like regions within the DG Of the annotated prophages from S. Enteritidis PT4 P125109 represented on the array one Kenyan and 4 Uruguayan isolates lacked ϕSE20 (Region 4 in our analysis), a ~41 kb phage similar to ϕST64B. Phage SE20 is thought to be intact

and a recent acquisition in S. Enteritidis PT4 P125109 and like ϕST64B, it carries fragments of the sopE and orgA genes, which have been implicated in Salmonella virulence [27, 29]. Two of the 4 Uruguayan isolates that lack ϕSE20 were isolated from human infections more than 5 years before the beginning of the epidemic in Uruguay (31/88 and 8/89), whereas the other 2 were from food samples, one from before (53/94) and the other from the middle (206/99) of the epidemic. Similarly, Porwollik and collaborators have reported that this phage https://www.selleckchem.com/products/Cyclopamine.html (called ϕST64B in their work) is absent in strains of S. Enteritidis isolated more than 50 years ago and suggested that acquisition of this phage may be related to the emergence of S. Enteritidis as being epidemic worldwide [21]. We corroborated the presence of ϕSE20 among the 29 Uruguayan isolates by PCR using two set of ϕSE20-specific primers that amplify fragments of sb9 and sb41 (SEN1935 and SEN1993 respectively). Only isolates 31/88, 8/89,

53/94 and 206/99 were negative validating IMP dehydrogenase the microarray results. We extended the PCR screening with sb41 primers to another 85 S. Enteritidis isolates from the original sample set, which included 28 isolates from human gastroenteritis, 30 isolates from invasive human disease and 27 isolates from non-human origin (including the 2 other pre-epidemic isolates that had not been included in the CGH analysis). Among them we found only 4 other isolates that lack sb41, i.e. 50/99 and 211/00 originating from food, 107/99 from enteric disease and 209/01 from invasive infection. In summary, we found that only 5 out of 108 isolates tested from the epidemic and post-epidemic periods lack ϕSE20, whereas 3 out of 6 pre-epidemic isolates lack this phage. This provides further support for the idea that the presence of ϕSE20 is a marker for the emergence of particular isolates as epidemic strains [21, 27]. It has been proposed that S.

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“Background In recent years, coagulase-negative Staphylococcus epidermidis ( Se)

has become the leading cause of infections related to indwelling medical devices such as vascular catheters, prosthetic joints and artificial heart valves [1, 2]. Pathogenicity of Se is attributed to its formation of biofilm on the surface of medical devices, thereby enhancing Se resistance to antibiotics and host defenses in this setting [3, 4]. In general, Se biofilm formation is a two-step process, in which bacteria first adhere to the surface (initial attachment phase) and subsequently form cell–cell aggregates and a multilayered architecture (accumulative phase) [5, 6]. One autolysin protein, AtlE, facilitates bacterial attachment to the surface of medical devices and dictates pathogenesis for Se biofilm-associated infections in vivo [7, 8]. In the accumulative phase, the polysaccharide intercellular adhesin (PIA), a linear poly-Nacetyl-1,6-β-glucosamine (PNAG) encoded by the icaADBC locus, is the major pathogenic determinant for intercellular adhesion [9, 10].

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