(PDF 106 KB) Additional file 2: Table S3 Proteins over-expressed

(PDF 106 KB) Additional file 2: Table S3. Proteins over-expressed in L. sakei MF1053. Presents buy VS-4718 the identification and characteristics of protein spots over-expressed in L. sakei MF1053 compared to the other L. sakei strains in this study. (PDF 42 KB) References 1. Katagiri H, Kitahara K, Fukami K: The characteristics of the lactic acid bacteria isolated from moto, yeast mashes for sake manufacture. Part IV. Classification of the lactic acid bacteria. Bulletin of Agricultural and Chemical Society of Japan 1934, 10:156–157. 2. Klaenhammer T, Altermann E, Arigoni F, Bolotin A, Breidt F, Broadbent J, Cano R, Chaillou S, Deutscher J, Gasson M, Guchte M, Guzzo J, Hartke A, Hawkins

T, Hols P, Hutkins R, Kleerebezem M, Kok J, Kuipers O, Lubbers M, Maguin E, McKay L, Mills D, Nauta A, Overbeek R, Pel H, Pridmore D, Saier M, van Sinderen D, Sorokin A, et al.: Discovering lactic acid bacteria by genomics. Antonie Van Leeuwenhoek 2002, 82:29–58.PubMedCrossRef 3. Vogel RF, Lohmann M, Nguyen M, Weller AN, Hammes WP: Molecular characterization of Lactobacillus curvatus and Lact. sake isolated from sauerkraut and their application in sausage fermentations. J Appl Bacteriol 1993, 74:295–300.PubMed 4. Leroi F, Joffraud JJ, Chevalier F, Cardinal M: Study of the microbial ecology of cold-smoked salmon

during storage at 8 degrees C. Int J Food Microbiol 1998, 39:111–121.PubMedCrossRef 5. Lyhs U, Bjorkroth J, Korkeala H: Characterisation of lactic acid bacteria from CP673451 purchase spoiled, vacuum-packaged, cold-smoked rainbow OICR-9429 ic50 trout using ribotyping. Int J Food Microbiol 1999, 52:77–84.PubMedCrossRef 6. Hammes WP, Bantleon A, Min S: Lactic acid bacteria in meat fermentation. FEMS Microbiol Rev 1990, 87:165–174.CrossRef 7. Hammes WP, Hertel C: New developments in meat starter cultures. Meat Science 1998, 49:125–138.CrossRef 8. Vermeiren L, Devlieghere F, Debevere J: Evaluation of meat born lactic acid bacteria as protective cultures for biopreservation

of cooked meat products. Int J Food Microbiol 2004, 96:149–164.PubMedCrossRef 9. Bredholt S, Nesbakken T, Holck A: Protective cultures inhibit growth of Listeria monocytogenes and Escherichia coli O157:H7 selleck chemicals in cooked, sliced, vacuum- and gas-packaged meat. Int J Food Microbiol 1999, 53:43–52.PubMedCrossRef 10. Bredholt S, Nesbakken T, Holck A: Industrial application of an antilisterial strain of Lactobacillus sakei as a protective culture and its effect on the sensory acceptability of cooked, sliced, vacuum-packaged meats. Int J Food Microbiol 2001, 66:191–196.PubMedCrossRef 11. Axelsson L, Ahrné S: Lactic acid bacteria. In Applied microbial systematics. Edited by: Priest FG, Goodfellow M. Dordrechet, The Netherlands: Kluwer Academic Press; 2000:365–386. 12. Chiaramonte F, Blugeon S, Chaillou S, Langella P, Zagorec M: Behavior of the meat-borne bacterium Lactobacillus sakei during its transit through the gastrointestinal tracts of axenic and conventional mice. Appl Environ Microbiol 2009, 75:4498–4505.PubMedCrossRef 13.

Potential for coordinated regulation of motility and virulence ge

Potential for coordinated regulation of motility and virulence gene expression Given the data presented in the current study, the concurrent lack of flagella and reduced toxin secretion in the flhA mutant Proteasome function is more consistent with a hypothesis of coordinated

regulation of motility and virulence genes, rather than FEA-dependent toxin secretion. This is also supported by the previously observed two-fold reduction in transcription of the genes encoding Hbl in the flhA mutant [11]. Coordinated regulation of motility and virulence genes has been demonstrated in several pathogenic bacteria (for reviews see e.g. [9, 42–44]). While diarrhoea due to B. cereus infection presumably occur through destruction of epithelial cells by enterotoxins produced in the small intestine [45, 46], the role of motility, if any, in B. cereus infection has not been investigated. Nevertheless, several studies suggest that a connection exists between expression of motility and virulence genes also in B. cereus and B. thuringiensis: First, an avirulent and non-flagellated B. thuringiensis mutant (Bt1302) showed greatly reduced phospholipase and haemolytic activity [47]. A spontaneous

suppressor mutation was able to reverse these phenotypes, Non-specific serine/threonine protein kinase and although motility was only partially restored, this indicated that these unidentified mutations affected a regulatory pathway shared between genes encoding Milciclib chemical structure flagellin, phospholipases, and haemolysins [47]. Bt1302 is not likely to be a flhA mutant, since their phenotypes differ, for example in expression of flagellin and RGFP966 datasheet growth rate at 37°C [11, 13, 47]. Second, PlcR, the transcriptional activator of B. cereus extracellular virulence factors, appears to also affect motility, as a plcR mutant showed reduced motility on agar plates

and reduced flagellin expression [10, 48]. Third, Hbl production was shown to increase during swarming migration [12, 49], a differentiated state where elongated and hyperflagellate swarm cells collectively move across solid surfaces [50]. Notably, it was shown that hbl genes were upregulated during swarming, concomitant with increased expression of flagellar genes, while the majority of other genes regulated by PlcR, including plcR, nhe, and cytK, were downregulated during swarming [49]. Interestingly, upregulation of the hbl operon concomitantly with downregulation of plcR, nhe and other PlcR-regulated genes was also observed in a deletion mutant of the two-component system yvfTU [51]. Finally, the non-flagellated B.

Data extraction Hazard Ratios (HR) for PFS

and OS and the

Data extraction Hazard Ratios (HR) for PFS

and OS and the number of events for secondary end-points were extracted; the last trial’s available update was considered as the original source. All data were reviewed and separately computed by four investigators (F.Cu., E.B., I.S., and D.G.). Data synthesis HRs were extracted from each single trial for primary end-points GS-9973 purchase [19, 20], and the log of relative risk ratio (RR) was estimated for secondary endpoints [21]; 95% Confidence Intervals (CI) were derived [22]. A random-effect model according to DerSimonian-Laird method was preferred to the fixed, given the known clinical heterogeneity of trials; a Q-statistic heterogeneity test was used. Absolute benefits for MK0683 ic50 each outcome were calculated (i.e. absolute benefit = exp HR or RR × log[control survival] – control survival [23]; modified by Parmar and Machin [24]). The number of patients needed to treat (or to harm one in

case of toxicity) for one single beneficial patient was determined (NNT or NNH: 1/[(Absolute Benefit)/100]) [25]. Results were depicted in all figures as conventional meta-analysis forest plots. In order to find possible correlations between outcome effect and negative prognostic factors (selected among trials’ reported factors: > 3 sites, no adjuvant CT, visceral site, hormonal receptors negative (RN), prior taxanes, T or anthracyclines, A) a meta-regression approach was adopted (i.e. regression of the selected predictor on the Log HR/RR of the corresponding outcome). Calculations were accomplished using the Comprehensive Meta-Analysis Software, version v. 2.0 (CMA, Biostat, Englewood, NJ, USA). Results Selected

trials Five trials (3,841 patients) were identified (Figure 1) [13, 14, 16, 26, 27], all included in the meta-analysis, and evaluable for PFS (primary outcome). The patients’ sample for each trial ranged from 462 to 736 patients cAMP (Table 1). One trial was conducted with a double comparison [16]. Trials characteristics are listed in Table 1; 2 RCTs evaluated the addition of Bevacizumab as second line treatment [26, 27], and one of these included patients who received 2 or more regimens of chemotherapy for metastatic disease [27]. One trial (462 patients) did not report survival data [27], so 4 RCTs were evaluable for OS (3,379 patients). With regard to secondary outcomes, all RCTs were evaluable for ORR, HTN, Bleeding, GSK1904529A Proteinuria and Thrombosis; 4 RCTs (3,379 patients) were evaluable for Neurotoxicity, Febrile Neutropenia, Gastro-intestinal perforation [13, 14, 16, 26].

267/3 672) Secondary variables were correlated with DCA axis in

267/3.672). Secondary variables were correlated with DCA axis in a post selleck screening library hoc manner (mean Ellenberg indicator

values (EIV) for moisture (F) and nutrients (N); species richness) References Ammermann K (2008) learn more Energetische Nutzung nachwachsender Rohstoffe. Auswirkungen auf die Biodiversität und Kulturlandschaft. Natur und Landschaft 83:108–110 Bakker JP, Berendse F (1999) Constraints in the restoration of ecological diversity in grassland and heathland communities. Trends Ecol Evol 14:63–68PubMedCrossRef Bauerkämper A (2004) The industrialization of agriculture and its consequences for the natural environment: an inter-German comparative perspective. Hist Soc Res 29:124–149 Benton TG, Vickery JA, Wilson JD (2003) Farmland biodiversity: is habitat heterogeneity the key? Trends Ecol Evol 18:182–188CrossRef Bergmeier E, Nowak B (1988) Rote Liste der Pflanzengesellschaften der Wiesen und Weiden Hessens. Vogel und Umwelt 5:23–33 Bignal EM, McCracken www.selleckchem.com/products/mk-5108-vx-689.html DI (2000) The nature conservation value of European traditional farming systems. Environ Rev 8:149–171CrossRef Bischoff A, Warthemann G, Klotz S (2009) Succession of floodplain grasslands following reduction in land use intensity: the importance of environmental conditions, management and dispersal. J Appl Ecol 46:241–249CrossRef Bissels S, Hölzel N, Donath

TW, Otte A (2004) Evaluation of restoration success in alluvial grasslands under contrasting flooding regimes. Biol Conserv 118:641–650CrossRef Boschi C, Baur B (2008) Past pasture management affects the land snail diversity in nutrient-poor calcareous grasslands. Basic Appl Ecol 9:752–761CrossRef Dierschke H, Briemle G (2002) Kulturgrasland. Ulmer, Stuttgart Dierßen K, von Glahn H, Härdtle W, Höper H, Mierwald U, Schrautzer J, Wolf A (1988) Rote Liste der Pflanzengesellschaften Schleswig-Holsteins. SchR Landesamt Natsch LandschPfl, vol 6.

Kiel Donald PF, Green RE, Heath MF (2001) Agricultural intensification and the collapse of Europe’s farmland bird populations. Proc R Soc Lond B 268:25–29CrossRef Ellenberg H, Leuschner C (2010) Vegetation Mitteleuropas mit den Alpen, 6th edn. Ulmer, Niclosamide Stuttgart European Commission (2007) Interpretation manual of European Union habitats EUR, vol 27. European Commission, Bruxelles Fischer W (1980) Beitrag zur Gründlandvegetation der Gülper Havelaue. Wissenschaftliche Zeitschrift Pädagogische Hochschule Karl Liebknecht 25:383–396 Gerard M, Kahloun MEl, Mertens W, Verhagen B, Meire P (2008) Impact of flooding on potential and realised grassland species richness. Plant Ecol 194:85–98CrossRef GIVD (2010) Global index of vegetation-plot databases. Reference no. EU-DE-009 BioChange Meadows. http://​www.​givd.​info/​ Grevilliot F, Krebs L, Muller S (1998) Comparative importance and interference of hydrological conditions and soil nutrient gradients in floristic biodiversity in flood meadows.

Pooled fractions were concentrated to 500 μl using nanosep 10 k c

Pooled fractions were concentrated to 500 μl using nanosep 10 k cutoff centrifugal device (Pall Life Sciences, MI, USA). In preparation for the MTT assay, the resultant fractions were diluted to 2 ml volumes with Sorenson’s buffer. Mass spectrometry (MS) Trypsin digests on excised gel bands were performed in a solution of 20 mM ammonium bicarbonate containing 0.5 μg trypsin (Promega corporation, Madison, WI, USA) and then LY294002 clinical trial analysed directly by LCMS as outlined below. Trypsin digests on the pool B fraction directly

were performed in a solution of 20 mM ammonium bicarbonate containing 10 μg trypsin (Promega corporation) and then the resultant digested MAPK inhibitor peptides were fractionated by 12 salt plug elutions ranging from 2 mM to 500 mM NaCl from a SCX TopTip (Glygen, Columbia, MD, USA) according to manufacturer’s instruction. Both digest protocols were incubated at 37°C for 12 hours. Tryptic digests were analysed by LC-MS/MS using the HCT ULTRA ion trap mass spectrometer (Bruker Daltonics, Bremen, Germany) coupled online with a 1200 series capillary HPLC (Agilent technologies). Samples were injected onto

a zorbax 300SB reversed phase column with buffer A (5% acetonitrile 0.1% formic acid) at a flow rate of 10 μl/minute. The peptides were eluted over a 30-minute gradient to 55% B (90% acetonitrile 0.1% formic acid). The eluant was nebulised and ionised using the Bruker electrospray source using the low flow electrospray needle with a capillary voltage of 4000 V dry gas at 300°C, flow AZD1152 clinical trial rate of 8 l/minute and nebuliser gas pressure at 1500 mbar. Peptides Chorioepithelioma were selected for MSMS analysis in autoMSn mode with smart parameter settings selected and active exclusion released after 1 minute. Data from LCMSMS runs were processed using Data Analysis 3.4 (Bruker Daltonics) and were exported in Mascot generic file format (*.mgf) and searched against an in-house database comprised of C. jejuni FASTA format genomes downloaded from the National Center for Biotechnology

Information (NCBI) FTP site using the MASCOT search engine (version 2.1, Matrix Science Inc., London, United Kingdom) using MUDPIT scoring. The mgf files from the salt plug elutions were combined into a single mgf file. The following search parameters were used: missed cleavages, 1; peptide mass tolerance, ± 0.4 Da; peptide fragment tolerance, ± 0.2 Da; peptide charge, 2+ and 3+; fixed modifications, carbamidomethyl; variable modification, oxidation (Met). Stability of cytotoxin to protease digestion The cytotoxin in pool B fraction was treated with trypsin (125 μg/ml) (Sigma, St. Louis, MO, USA) for 4 h at 37°C. The trypsin was inactivated by the addition of 125 μg/ml soybean trypsin inhibitor (Sigma). One hundred microliters of treated pool B fractions at a concentration of 2 μg/ml were added to a CHO cell monolayer in a microtitre plate. The MTT assay [9] for cytotoxicity was performed after a 24 h incubation period.

The athletes were contacted by the researchers via phone between

The subjects had 12.9 ± 8.8 years of experience in endurance events, and their average weekly training volume was from 15 hours up to a maximum of 30 hours, with a total volume between 800 and 1,000 hours per year. They were all members of the Spanish Cycling or Triathlon Federations and, up to the start of the study, reported no related I-BET-762 clinical trial medical illnesses. All the subjects passed a medical examination and gave their informed written consent, approved by the Ethics Committee of the Catalonian Sports Council, prior https://www.selleckchem.com/products/Nilotinib.html to their participation. Table 1 Physical and physiological selleck products characteristics of the subjects Subjects 1 2 3 4 5 6 7 8 M ± SD Age (years) 34.4 39.7 29.6 38.3 43.3 39.8 31.0 37.5 36.7 ± 4.7 Height (cm) 167.0 172.4 189.1 165.1 177.6 173.5 176.0 176.0 174.6 ± 7.3 Body mass (kg) 65.3 68.9 79.9 65.7 73.9 74.5 72.5 72.4 71.6 ± 4.9 BMI (kg·m2) 23.4 23.2 22.3 24.1 23.4 24.7 23.4 23.4 23.5 ± 0.5 Body fat (%) 9.5 10.8 9.7 11.1 9.2 10.4 9.8 10.6 10.1 ± 0.7 VO2peak (mL·kg-1·min-1) 70.2 71.9 62.5 53.1 69.1 56.4 74.7 69.2 66.4 ± 6.8 HRmax (bpm) 184 165 177 165 178 174 176 176 174 ± 9 VT (% HRmax) 72 74 75 83 74 77 80 85 77 ± 5 RCP (% HRmax) 91 89 90 89 91 89 90 92 90 ± 1 Wpeak (W·kg-1) 6.1 6.2 6.3 5.7 6.4 6.0 5.5

5.9 6.0 ± 0.3 BMI: body mass index; VO2peak: oxyclozanide peak of oxygen uptake; HRmax: maximum heart rate; VT: ventilatory threshold expressed as % of HRmax; RCP: respiratory compensation point expressed as % of the maximum heart rate; Wpeak: peak of power. Preliminary testing One week prior to the competition, all our athletes reported to a physiology

laboratory to perform an incremental VO2max test under controlled conditions (22 ± 1°C, 40 – 60% relative humidity, 760 – 770 mmHg barometric pressure). They were asked to refrain from caffeine, alcohol and heavy exercise on the day before the tests, and to report to the laboratory at least two hours after having eaten. An incremental test was performed on an electronically braked cycle ergometer (Excalibur Sport, Lode, The Netherlands) modified with clip-on pedals. The exercise protocol started at 25 watts (W) and was increased by 25 W every minute until voluntary exhaustion. The pedaling cadence was individually chosen within the range of 70 – 100 revolutions per minute (rpm). During the test, oxygen uptake (VO2), minute ventilation (VE), carbon dioxide production (VCO2) and respiratory exchange ratio (RER) were measured, breath-by-breath, using a computerized gas analyzer (Cosmed Quark PFT-Ergo, Italy). Before each test, the ambient conditions were measured and the gas analyzers and inspiratory flowmeter were calibrated using high-precision calibration gases (16.00 ± 0.01% O2 and 5.

In light of this and inspired by the remarkable pharmaceutical an

In light of this and inspired by the remarkable pharmaceutical and agricultural potential of bioactive metabolites of actinobacteria, Kaur et al. [29] screened actinobacterial isolates, recovered from

different rhizospheric and non-rhizospheric soils, for antifungal activity against fungal phytopathogens and reported strong insecticidal activity against S. litura in one of the isolates, Streptomyces hydrogenans DH16 which also exhibited potent antifungal activity [30]. Present study was aimed at further systematic evaluation of antifeedant, larvicidal, pupicidal and growth inhibitory effect of solvent extract from S. hydrogenans DH16 against S. litura. Results and discussion There is a long history of utilizing natural products produced by microbes for pharmaceutical and agricultural purposes. Actinobacteria especially, Streptomyces Selleckchem 4SC-202 spp. have provided wide variety of secondary metabolites of high commercial importance and continue to be APR-246 manufacturer routinely screened for new bioactive compounds. Present work further corroborates the earlier findings CP673451 and reports that secondary metabolites from S. hydrogenans exhibit the potential to be used as insecticidal agents. In this study, S. hydrogenans extract showed deleterious effects on growth and

development of S. litura larvae that survived the toxic effects of highest concentration. Significant increase in larval development period was observed at all concentrations over the control (P ≤ 0.05). At highest concentration (1600 μg/ml), larval period prolonged by 6.24 days in comparison to control group (Table 1). Our result

coincided with the findings of Arasu et al. [21] who reported larvicidal and growth inhibitory activities of a novel polyketide metabolite isolated from Streptomyces sp. AP-123 against H. armigera and S. litura. The metabolite also prolonged the larval–pupal duration of the insects at all the tested concentrations as compared to control. The delayed larval period observed in the present study could be due to low consumption Parvulin of diet by the larvae of S. litura indicating the antifeedant effect of the extract. Pupal period decreased significantly with treatment (P ≤ 0.01) however, at highest concentration pupae formed from treated larvae remained in pupal stage till the termination of experiment. The total development period from larva to adult of S. litura differed but remained non significant (Table 1). The LC50 and LC90 values were 1337.384 and 2070.516 μg/ml, respectively for S. litura (Table 2). No larval mortality was observed in lowest concentration as well as in control but when larvae were fed on highest concentrations of 800 and 1600 μg/ml, larval mortality of 20 and 70%, respectively was recorded and was statistically significant compared to control (P ≤ 0.01).

PubMed 37 Weston A, Godbold JH: Polymorphisms of H-ras-1 and p53

PubMed 37. Weston A, Godbold JH: Polymorphisms of H-ras-1 and p53 in breast cancer and lung cancer: a meta-analysis. Environ Health Perspect 1997, 105 (Suppl 4) : 919–926.CrossRefPubMed 38. Papadakis EN, Dokianakis DN, Spandidos DA: p53 codon 72 polymorphism as a risk factor in the development of breast cancer. Mol Cell Biol Res Commun 2000, 3: 389–392.CrossRefPubMed 39. Noma C, Miyoshi Y, Taguchi T, Tamaki Y, Noguchi S: Association of p53 genetic polymorphism (Arg72Pro) with estrogen receptor positive breast cancer risk in Japanese women. Cancer Lett 2004, 210: 197–203.CrossRefPubMed

40. buy Barasertib Ohayon T, Gershoni-Baruch R, Papa MZ, Distelman Menachem T, Eisenberg Barzilai S, Friedman E: The R72P P53 mutation is associated with familial breast cancer in Jewish women. Br J Cancer 2005, 92: 1144–1148.CrossRefPubMed check details 41. Damin AP, Frazzon AP, Damin DC, Roehe

A, Hermes V, Zettler C, Alexandre CO: Evidence for an association of TP53 codon 72 polymorphism with breast cancer risk. Cancer Detect Prev 2006, 30: 523–529.CrossRefPubMed 42. Costa S, Pinto D, Pereira D, Rodrigues H, Cameselle-Teijeiro J, Medeiros R, Schmitt F: Importance of TP53 codon 72 and intron 3 duplication 16 bp polymorphisms in prediction of susceptibility on breast cancer. BMC Cancer 2008, 8: 32.CrossRefPubMed 43. Själander A, Birgander R, Hallmans G, Cajander S, Lenner P, Athlin L, Beckman G, Beckman L: p53 polymorphisms and haplotypes in breast signaling pathway cancer. Carcinogenesis 1996, 17: 1313–1316.CrossRefPubMed 44. Weston A, Pan CF, Ksieski HB, Wallenstein S, Berkowitz GS, Tartter PI, Bleiweiss IJ, Brower ST, Senie RT, Wolff MS: p53 haplotype determination in breast cancer. Cancer Epidemiol Biomarkers Prev 1997, 6: 105–112.PubMed 45. Li T, Lu ZM, Guo M, Wu QJ, Chen KN, Xing HP, Mei Q, Ke Y:

p53 codon C1GALT1 72 polymorphism (C/G) and the risk of human papillomavirus-associated carcinomas in China. Cancer 2002, 95: 2571–2576.CrossRefPubMed 46. Wang-Gohrke S, Becher H, Kreienberg R, Runnebaum IB, Chang-Claude J: Intron 3 16 bp duplication polymorphism of p53 is associated with an increased risk for breast cancer by the age of 50 years. Pharmacogenetics 2002, 12: 269–272.CrossRefPubMed 47. Buyru N, Tigli H, Dalay N: P53 codon 72 polymorphism in breast cancer. Oncol Rep 2003, 10: 711–714.PubMed 48. Huang XE, Hamajima N, Katsuda N, Matsuo K, Hirose K, Mizutani M, Iwata H, Miura S, Xiang J, Tokudome S, Tajima K: Association of p53 codon Arg72Pro and p73 G4C14-to-A4T14 at exon 2 genetic polymorphisms with the risk of Japanese breast cancer. Breast Cancer 2003, 10: 307–311.CrossRefPubMed 49. Katiyar S, Thelma BK, Murthy NS, Hedau S, Jain N, Gopalkrishna V, Husain SA, Das BC: Polymorphism of the p53 codon 72 Arg/Pro and the risk of HPV type 16/18-associated cervical and oral cancer in India. Mol Cell Biochem 2003, 252: 117–124.CrossRefPubMed 50.

In contrast to other loci, the distribution of ter foci clearly d

In contrast to other loci, the distribution of ter foci clearly differed between the two cell populations (p-value < 10-3; Figure 3). The distribution of foci in cells with a SRT1720 single focus appeared more peripheral than random. Indeed, the distribution was significantly different from the random and central models (p-value < 10-3); the best fitting model was the 90% central 60% peripheral model in which foci are excluded from Ion Channel Ligand Library order the 10% cell periphery and 40%

cell centre regions (p-value = 0.1; Figure 3). Cells with two foci showed a distribution more central than random. It was however different from any simulated distribution (p-value < 0.05). This more central location is not due to local deformation of the membrane during constriction of the division septum since cells with a constricting septum were omitted from our analysis. The ter region is the last to be segregated, and consequently nucleoid segregation is almost completed when ter foci are duplicated [8]. It follows that duplicated ter foci located close to midcell lie at the mid-cell edge of the nucleoid. The distributions of foci of the ter locus in cells harbouring one or two foci thus indicates that the ter region is preferentially located at the periphery of the nucleoid, either close to the parietal membrane (in single foci cells) or close to a cell pole (after ter duplication) throughout

cell cycle progression. To rule out a specific behaviour of Tipifarnib the ter locus used, we analysed a second ter locus located at 1490 kb (trg). The results reported in Additional file1 Figure S5 clearly show that the trg locus also preferentially

localises at the nucleoid periphery in the cell population harbouring a single fluorescent focus. This strongly suggests that the peripheral location C-X-C chemokine receptor type 7 (CXCR-7) is a general property of the terminal region of the chromosome. Loci positioning after nucleoid disruption We tested whether the same approach could detect a change in chromosome organisation. We used production of the Ndd (Nucleoid Disruption Determinant) protein from the T4 bacteriophage. Ndd disrupts the central and compacted structure of the nucleoid in E. coli and causes chromosomal DNA to delocalise to the cell periphery [22–24]. A plasmid carrying a T7p- ndd2 Ts fusion was transferred into the strains carrying parS insertions, which express the T7 RNA polymerase (Methods). Strains containing the pT7- ndd2 Ts plasmid had a doubling time similar to the parental strains in the absence of Ndd production (45 min. at 42°C in M9 medium). Ndd2Ts production was induced by a rapid temperature shift down to 30°C in the presence of IPTG (Methods). Ndd2Ts-producing cells (hereafter called Ndd-treated cells) stopped dividing almost immediately and did not elongate more than 1 μm (not shown; [25]). The DNA was stained with DAPI and the cells examined by microscopy.

2 Bardeen J: Surface states and rectification at a metal semi-co

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