This model showed hepatopathy, including hepatic steatosis and liver tumors. In this study, we describe

a model to examine immune-mediated liver cell damage by means of adoptive transfer of splenocytes from HCV immunized mice into HCV transgenic mice. Our results showed that the carboxyfluorescein succinimidyl ester (CFSE)-labeled T cells from HCV immunized mice homed to the liver of HCV transgenic mice, indicating that these HCV-activated T cells recognize the HCV transgene and attack the hepatocytes expressing it, which may lead to liver damage. Methods Mice All mice used in the study were purchased from the Charles River Laboratories (Senneville, QC, Canada) and were from

a B6C 3F1 genetic background. Mice were bred in specific pathogen-free conditions at the animal care facilities at the University of Ottawa. Animals were Cabozantinib used according to the guidelines of the animal care committee at the University of Ottawa. Donor mice were 6 to 8 weeks old; wild type mice and the recipient mice, both HCV transgenic and non-transgenic mice, were 3 to 6 months old. The establishment and characterization of these HCV transgenic mice were described buy ZD1839 in our previous study [17]. Plasmids and proteins Construction of pVAX Core, E1 and E2 expression vector was described in our previous study [17]. Briefly, total RNA extracted from the from plasma of a patient infected with HCV genotype 1a was used as a template to amplify Core, E1, and E2 genes. The HCV fragment containing Core, E1, and truncated E2 genes was constructed

through RT-PCR using forward primer 5′ ACC ATG AGC ACG AAT CCT AAA CCTC 3′ and reverse primer 5′ TGG TAG GGT TGT GAA GGA ACA CG 3′. The amplified fragment was cloned into the EcoR1 sites of pCR 2.1 vector using the TOPO-TA cloning kit (Invitrogen, Burlington, ON). The nucleotide sequence was verified by DNA sequencing using the University of Ottawa DNA sequencing facility. The Core, E1, E2 fragment was subsequently subcloned into pVAX-1 plasmid (Invitrogen, Burlington, ON) downstream of a cytomegalovirus promoter. The expression vector of recombinant HCV Core, E1 and E2 polyprotein was also described in our previous study [18]. Briefly, the TOPO-TA HCVcore/E1/E2 construct was subcloned into the pEF6/Myc-His expression vector (Invitrogen Burlington, ON); this vector contains six histidine residues which permit purification of the HCV polyprotein by immobilized metal affinity chromatography (Clontech Talon Metal Affinity Resin Kit, Palo Alto, CA). The recombinant plasmid containing the correctly oriented insert was transfected into DH5 cells, amplified, and purified using the Endofree plasmid purification kit (Qiagen), as previously described.

Br J Cancer 1996, 74:753–758.PubMedCrossRef 11. Flanders KC, Wakefield LM: Transforming growth factor-(beta)s and mammary gland involution; functional roles and

implications for cancer progression. J Mammary Gland Biol Neoplasia 2009, 14:131–144.PubMedCrossRef 12. Ito M, Minamiya Y, Kawai H, Saito S, Saito H, Nakagawa T, Imai K, Hirokawa M, Ogawa J: Tumor-derived TGF beta-1 induces dendritic cell apoptosis in the sentinel lymph node. J Immunol 2006, 176:5637–5643.PubMed 13. Halliday GM, Le S: Transforming growth factor-beta produced by progressor tumors inhibits, while IL-10 produced by regressor tumors enhances, Langerhans cell migration Selleck Temozolomide from skin. Int Immunol 2001, 13:1147–1154.PubMedCrossRef 14. Byrne SN, Halliday GM: Dendritic cells: making progress with tumour regression? Immunol Cell Biol 2002, 80:520–530.PubMedCrossRef 15. Cui Erlotinib cell line W, Fowlis DJ, Bryson S, Duffie E, Ireland H, Balmain A, Akhurst RJ: TGFb1 inhibits the formation of benign skin tumors, but enhances progression to invasive spindle carcinomas in transgenic mice. Cell 1996, 86:531–542.PubMedCrossRef 16. Labeur MS, Roters B, Pers B, Mehling A, Luger TA, Schwarz T, Grabbe S: Generation of tumor immunity by bone marrow-derived dendritic cells correlates with dendritic cell maturation stage. J Immunol 1999, 162:168–175.PubMed 17. Ogata M, Zhang Y, Wang Y, Itakura

M, Zhang YY, Harada A, Hashimoto S, Matsushima K: Chemotactic response toward chemokines and its regulation by transforming growth factor-beta1 of murine bone marrow hematopoietic progenitor cell-derived different subset of dendritic cells. Blood 1999, 93:3225–3232.PubMed 18. Saito H, Tsujitani S, Oka S, Kondo

A, Ikeguchi M, Maeta M, Kaibara N: An elevated serum level of transforming growth factor-beta 1 (TGF-beta 1) significantly correlated with lymph node metastasis and poor prognosis in patients with gastric carcinoma. Anticancer Res 2000, 20:4489–4493.PubMed 19. Meulmeester E, Ten Dijke P: The dynamic roles of TGF-β in cancer. J Pathol 2011, 223:205–218.PubMedCrossRef 20. Weber F, Byrne SN, Le S, Brown DA, Breit SN, Scolyer RA, Halliday GM: Transforming growth factor-beta1 immobilises dendritic cells within skin tumours and Chorioepithelioma facilitates tumour escape from the immune system. Cancer Immunol Immunother 2005, 54:898–906.PubMedCrossRef 21. Padua D, Massagué J: Roles of TGF beta in metastasis. Cell Res 2009, 19:89–102.PubMedCrossRef 22. Cheng N, Bhowmick NA, Chytil A, Gorksa AE, Brown KA, Muraoka R, Arteaga CL, Neilson EG, Hayward SW, Moses HL: Loss of TGF-beta type II receptor in fibroblasts promotes mammary carcinoma growth and invasion through upregulation of TGF-alpha-, MSP-and HGF-mediated signaling networks. Oncogene 2005, 24:5053–5068.PubMedCrossRef 23.

There is still some way to go to reach this aim. In the framework of this paper our descriptions of the wood-pasture categories have to be brief and general. Specific local types may not always be covered, as our categories cannot describe the full range of intermediates that exist. This survey is based on geobotanical criteria used for woodlands and grasslands alike, such as climatic zone,

altitudinal belt, physiognomy, and dominant species. The major bioclimatic zones in Europe are boreal, meaning the northern conifer-dominated taiga zone, nemoral, comprising the temperate and submeridional broadleaved forest zone, and meridional for the sclerophytic Mediterranean forest zone (Schroeder

1998). Hemiboreal (or boreonemoral), with its deciduous and coniferous woodlands, DAPT research buy is the transition zone between the first two, and submeridional, Erlotinib price with its chiefly thermophytic deciduous woodlands, between the temperate and the meridional zone. The wooded altitudinal belts are lowland, colline, submontane, montane, altimontane. In the meridional zone the altitudinal belts thermo-, meso-, supra- and oro-mediterranean are arranged using criteria of temperature and distance from coast. For further characteristics see Table 1. Table 1 Survey and characteristics of European wood-pasture habitats Wood-pasture habitat type Predominant trees Traditional land-use Landscape type, potential natural vegetation Animals Trees and ground

1 Quercus petraea, Q. robur Cattle, sheep Coppicing, lopping, barking Quercetalia roboris 2 Corylus avellana, Populus tremula, Fraxinus excelsior, Quercus robur, Tilia cordata Cattle Pollarding, coppicing, grass cutting, shredding, cultiv.fields Fagetalia, Vaccinio-Piceetalia 3 Betula pubescens s.l., Fraxinus excelsior, Picea abies, Quercus robur Cattle, sheep Coppicing, lopping Cladonio-Vaccinietalia 4 Betula pubescens s.l., Pinus sylvestris Reindeer   Cladonio-Vaccinietalia 5 Fagus sylvatica, Quercus petraea, Q. robur, Carpinus betulus Cattle, pigs, sheep, deer, horses Pollarding, lopping, shredding Fagetalia 6 Fagus sylvatica, Picea abies, Acer pseudoplatanus Cattle, sheep Lopping, grass cutting Fagetalia, Vaccinio-Piceetalia 7 Quercus robur, Q. petraea, Q. pyrenaica, Carpinus betulus, enough Pinus sylvestris Sheep, cattle, horses Pollarding, shredding, bee-keeping Quercetalia roboris 8 Quercus pubescens, Q. petraea agg., Q. frainetto, Q. cerris, Castanea sativa Sheep, cattle, pigs Pollarding, shredding, acorn collecting Quercetalia pubescentis 9 Q. robur s.l., Ulmus spp., Fraxinus excelsior, F. angustifolia s.l. Cattle, pigs, horses Pollarding, shredding, grass cutting Fagetalia 10 Larix decidua, Pinus cembra, P. uncinata Cattle, sheep Grass cutting Vaccinio-Piceetalia 11 Pinus heldreichii, P. sylvestris, Abies alba, A. borisii-regis, A. cephalonica, A.

Figure 1 Total ion chromatogram of crude serum organic extract. (A) Total ion current of bulk serum following liquid/liquid extraction and HPLC-coupled mass spectrometry as explained in the methods. (B) Extracted mass spectra of all masses from (A). (C) Extracted ion chromatograms of GTAs 446, 448 and 450 from the total ion current shown in A. (D) Cell proliferation, as assayed by MTT, for SW620 cells treated with up to 80 ug/ml of the crude serum extract. Organic serum extract was next subjected to flash

column chromatography as described in the methods, resulting in 12 fractions which were subsequently analyzed by selleck products HPLC-MS to determine GTA content. Although other components were present in all the fractions, only fraction 9 out of the 12 was enriched for the C28 GTAs (referred to as the GTA+ve fraction). A GTA negative control fraction (fraction 8, lacking any detectable GTAs) was also selected click here for the studies described below. Representative total ion chromatograms, extracted mass spectra and selected ion chromatograms of the three C28 GTAs for the GTA-ve and GTA+ve fractions are shown in Figures 2A and 2B, respectively. By comparing the sums of the selected ion chromatograms of the three GTAs to the total ion currents, we estimated that the GTA+ve fraction contained approximately 21% C28 GTAs while the GTA-ve fraction had no detectable

levels (bottom panel of Figures 2A and 2B). The non-GTA background components for both fractions were similar, and the most abundant non-GTA components in the GTA+ve fraction were also the most abundant components in the GTA-ve fraction. Therefore, the two fractions were compositionally similar

other than the 21% GTA content of the GTA+ve fraction, which represented an approximately 143-fold enrichment isothipendyl of the three C28 GTA metabolites over the crude organic serum extract (as shown in Figure 1A). These fractionations were repeated several times with consistent results. We therefore concluded that the fractions were sufficiently matched for investigating biological activity as described below. For comparison, the relative levels of the three C28 GTAs from 40 pooled CRC patients’ serum and serum from 40 matched control subjects is shown in Figure 2C. Figure 2 Mass spectrometry characterization of semi-purified GTA-ve and GTA+ve extracts. (A) Crude serum extract (as shown in Figure 1) was subject to flash column chromatography as described in the methods resulting in two adjacent eluates, one positive and one negative for the presence of GTAs. The total ion chromatogram (top), extracted mass spectra (middle), and extracted ion chromatograms for three GTAs (GTA446, 448 and 450; bottom) of the GTA-ve fraction. (B) Same as (A) for the GTA+ve fraction. (C) For comparison, the extracted ion chromatograms of GTA446, 448 and 450 from the extracts of serum pooled from 20 CRC patients and 20 controls is shown.

2 S.D. with 34.9% similarity and 24.8% identity (Additional file 1: Figure S9). These results indicate that in this

case, the six TMS porter lost one TMS at its C-terminus to give rise to the five TMS porter. Thus, at least two events gave rise to a 5-TMS topology from a primordial 6 TMS protein, one in which the N-terminal TMS was lost, and one in which the C-terminal was Belnacasan ic50 lost. Understanding the relationships between putative six and seven TMS porters To demonstrate the relationship between transporters that exhibit six or seven predicted TMSs, two proteins were chosen: MalG (TC# 3.A.1.1.1), a six TMS porter, and TogN (TC# 3.A.1.1.11), a putative seven TMS porter. The topological predictions obtained by WHAT and HMMTOP for the latter protein both gave seven TMSs; however, TMHMM predicted this protein to be a six TMS porter. The six TMS topology is also confirmed by TOPCONS and SPOCTUPUS, which according to our unpublished evaluations are the most reliable topological prediction programs currently AG-014699 mouse available. The hydropathy plot of TogN obtained with the WHAT program is shown in Additional file 1: Figure S10. We obtained the top twenty non-redundant homologues of this protein and used WHAT and TMHMM to predict the topology of each of these homologues. The results are presented in Additional file 1: Table S2. The top

twenty non-redundant hits to TogN were examined using the AveHAS program (see TCDB). The average hydropathy plot for these proteins is shown in Additional file 1: Figure S11. TogN (TC# 3.A.1.1.11), the putative seven TMS porter, aligned with the six TMS MalG homologue, gi134098247. TMSs 1–3 of both proteins aligned, giving a comparison score of 19 S.D. with 30% similarity and 21.9% identity (Additional file 1: Figure S12). TMSs 4–6 of MalG aligned with TMSs

4–7 of the TogN homologue, gi239820911. The result (Additional file 1: Figure S13) gave a comparison score of 22.4 S.D. with 44.4% similarity and 22.3% identity. We suggest that both proteins have 6 TMSs, and that the 7 TMS prediction is not accurate. Thus, sequences similar to ABC porters predicted to have 17-DMAG (Alvespimycin) HCl 7 TMSs may have 6 TMSs. Understanding the relationships between putative six and ten TMS transporters MalG (TC# 3.A.1.1.1), a six TMS transport protein, was aligned with the putative ten TMS protein RnsC (TC# 3.A.1.2.12) to elucidate the relationship between six and ten TMS porters. Homologues of both MalG and RnsC were aligned with MalG and RnsC, respectively, using the GAP and multiple sequence alignment programs to verify that their TMSs aligned in a pattern that would reveal their evolutionary relationships. Then, TMSs 1–3 of a MalG homologue (gi108803469) were aligned with TMSs 1–3 of the RnsC homologue (gi126656877) using GAP. The output gave a comparison score of 11.2 S.D. with 42.6% similarity and 30.9% identity (Figure 7). We conclude that the fourth and fifth TMSs of the RnsC homologue are extra TMSs.

Twenty-four hour after transfection, cells were incubated with chemotherapeutic agents for additional 24 hr (Doxo) and 48 hr (5-FU and Gem). The cytotoxicity was evaluated by SRB assay. Data represent

mean ± SEM, each from three separated experiments. *p < 0.05 vs the control vector transfected cells. Over-expression of NQO1 suppresses chemotherapeutic agents-induced p53 and protein expression in the cell death pathway Previous experiment showed that NQO1-knockdown increased p53 and apoptogenic protein expression. The results of this experiment showed that over-expression of NQO1 in KKU-M214 cells strongly suppressed the chemotherapeutic agents-induced increased expression of p53, p21, and Bax (Figure 5A-B & D). On the other hand, over-expression of NQO1 enhanced Doxo- and Gem-induced cyclin D1 expression (Figure 5C). Figure 5 NQO1 over-expression attenuates the p53 pathway in KKU-M214 cells. A-D, Western blots BMS-907351 in vivo of p53 (A), p21 (B), cyclin D1 (C), and Bax (D) protein in KKU-M214-NQO1

over-expressed cells after treatment with 5-FU 3 μM (48 hr), Doxo 0.1 μM (24 hr), and Gem 0.1 μM (48 hr). The relative bars that were normalized with β-actin of each band are shown below the Western blot images. *p < 0.05 vs the treated control vector Afatinib in vivo transfected cells. **p < 0.05 vs the untreated control vector transfected cells. Knockdown of p53 abolishes the chemosensitizing effect of NQO1 silencing Since the results given above showed that the knockdown and over-expression of NQO1 enhanced and suppressed, respectively, the chemotherapeutic agent-mediated cytotoxicity in association with the altered expression of p53, p53 apparently play a role in the expression of the cytotoxic effect of those anti-cancer agents. To validate the role of p53, we prepared the double knockdown of NQO1 and p53 in KKU-100 cells. The efficiency of NQO1 and

p53 knockdown was more than 80% (Figure 6A). As is shown above, NQO1-knockdown increased the susceptibility of KKU-100 cells to chemotherapeutic agents. Conversely, p53-knockdown markedly reduced cytotoxic effect of all tested chemotherapeutic agents compared with chemotherapeutic agents alone (Figure 6B-D). Interestingly, in the double knockdown experiment, the cytotoxic potentiation effect of NQO1 gene silencing was totally diminished by the simultaneous Adenosine knockdown of p53. The cytotoxic effects of chemotherapeutic agents on double knockdown cells were similar to those on p53 knockdown cells. These results strongly suggest that the cytotoxic effects of all 3 chemotherapeutic agents on CCA cells were dependent on p53 expression and NQO1 is probably the upstream modulator of p53. Figure 6 Double knockdown of NQO1 and p53 by siRNA altered KKU-100 cells to chemotherapeutic agents. (A) Effect of co-transfected NQO1 and p53 siRNA in KKU-100 cells. Cells were transfected with the pooled siRNA against NQO1 and p53 for 24 hr. The bars represent relative expression of NQO1 and p53 normalized with β-actin as internal control.

EHEC colonization of enterocytes of the large bowel is characterized by an intestinal attaching and effacing (A/E) histopathology, which is manifested by a localized degeneration of brush border microvilli and an intimate attachment of bacteria to actin-rich pedestal-like structures formed on the apical membrane directly beneath adherent bacteria [3]. The A/E lesion is due to the activity of a type III secretion

system (T3SS) mainly encoded by the 35–45 kb locus of enterocyte effacement pathogenicity island (hereafter named LEE), which is conserved in some EHEC isolates and other A/E pathogens such as enteropathogenic Escherichia coli (EPEC), atypical EPEC, rabbit EPEC, Escherichia albertii and Citrobacter rodentium[4–7]. The LEE pathogenicity island comprises PD-0332991 datasheet at least 41 genes that mainly are located in five major operons (LEE1 5). The LEE encodes see more a TTSS, translocator proteins, secreted effectors, regulators, an intimin (adhesin) and a translocated intimin receptor. The LEE-encoded regulators Ler, Mpc, GrlR

and GrlA are required for proper transcriptional regulation of both LEE- and non-LEE-encoded virulence genes in response to environmental cues [8–12]. The LEE was acquired by horizontal gene transfer [13] and is regulated by both generic E. coli- and pathogen-specific transcription factors. Consequently, the regulation of the LEE reflects characteristics of such genetic elements (For review see [11, 14]). Silencing of xenogeneic DNA in bacterial pathogens under conditions unfavorable for infection is important to ensure bacterial fitness [15]. H-NS, which is an abundant pleiotropic negative modulator of genes involved in environmental adaptation and virulence [16–20], is a major silencing factor of

horizontally acquired genes [21, 22]. H-NS GBA3 silences genes in the H-NS regulon by various mechanisms. Binding of H-NS to regulatory regions of these genes prevents RNA polymerase from accessing and escaping from promoter DNA, which represents two different mechanisms used by H-NS to silence gene expression (see [23–25] and references therein). H-NS is also a major transcriptional modulator of the LEE pathogenicity island, where it negatively affects the expression of LEE1-5, map and grlRA[26–31]. Further, H-NS binds to regulatory sequences upstream of virulence-associated genes located outside of the LEE including those encoding the long polar fimbriae (lpf) required for intestine cell adherence and enterohemolysin (ehx) [32, 33]. The expression of EHEC virulence genes including those encoded by the LEE is derepressed from the H-NS-mediated transcriptional silencing under physiological conditions that EHEC encounters during infection. Also, LEE expression is growth phase-dependent with maximum expression in early stationary phase [34].

In order to assess the potential of the microwave-assisted LBZA synthesis process for practical ZnO applications, we fabricated DSCs using the ZnO NSs produced by air annealing the LBZA NSs at

400°C in air to replace the traditional TiO2 NP scaffold. Figure 7a shows the current voltage characteristics of a DSC under one sun illumination. The open circuit voltage, short circuit current density and fill factor were 0.67 V, 5.38 mA/cm2 and 35.6%, respectively. The quantum efficiency (incident photon to charge carrier efficiency) as a function of wavelength is shown on Figure 7b. The characteristic dye absorption peaks can be seen at 410 and 525 nm, as well as the ZnO band edge absorption at 370 nm. The overall efficiency was 1.3%, better Napabucasin research buy than some previously reported ZnO nanowire DSCs [21] and compares well cells made with very high aspect ratio ZnO NWs (1.5%) [22] but still lower than cells based on hierarchical ZnO, where the high surface-to-volume ratio led to efficiencies of 2.63% [23]. It should be noted that the thickness of the ZnO NSs film could not be controlled accurately in this initial experiment, resulting in varying degree of dye loading. In the future, we look to improve the efficiency by optimizing the thickness and exploring different dyes. Figure 7 Performance of a 1-cm 2 DSC fabricated with ZnO NSs. (a) Current–voltage curve of the DSC recorded under one sun

illumination, yielding a short circuit current density of 5.38 mA/cm2, an open circuit voltage

of 0.67 V and a fill factor of 35.6%. The inset shows click here the DSC. The NSs were produced by annealing LBZA NSs at 400°C. (b) The incident photon to charge carrier efficiency as a function of wavelength for the cell. We also fabricated resistive (-)-p-Bromotetramisole Oxalate gas sensing devices using the same material with Figure 8 showing the effect of CO exposure on the resistance of a film of ZnO NSs obtained by annealing LBZA NSs at 400°C. The graph shows that the response, defined as R(air)/R(CO), was 1.65, 1.48, 1.32, 1.22 and 1.13 at 200, 100, 50, 25 and 12.5 ppm of CO, respectively. The response time was under 30 s for 100 ppm, whilst the recovery time was 40 s. Figure 8 demonstrates the stability of the sensing and highlights the potential of the material for this application. The sensitivity could be improved further by optimization of the thickness and cohesion of the films using organic binders. Figure 8 Resistance response to CO of a film of ZnO NSs at 350°C. The blue solid line shows the resistance versus time curve as various CO concentrations are mixed with the flowing dry air of the test chamber. The decreasing CO concentrations, from 200 to 12.5 ppm, are shown by the dashed red line. The inset shows the response of the sensing film as a function of CO concentration. Conclusion We report a novel technique for the production of ZnO nanocrystalline NSs through thermal decomposition of LBZA NSs.

The PCR products were subsequently verified by gel electrophoresis and purified by High Pure PCR Purification Kit (Roche Applied Sciences, Mannheim, Germany). The purified PCR product (200 ng) was digested with 2.0 μl of the restriction enzyme HhaI (Promega Corporation, Madison, USA) at 37°C for 3 h. Two μl of the digested PCR products, 10 μl formamide and 0.50 μl Megabase ET900-R Size Standard (GE Health Care, Buckinghamshire, UK) were mixed and run in duplicates on a capillary electrophoresis genetic analyzer (Genetic Analyzer 3130/3130xl, Applied Biosystems, Carlsberg, BIBW2992 CA). The terminal restriction fragments

(T-RFs), representing bacterial fragments in base pair (bp), were obtained and the analysis of T-RF profiles and alignment of T-RFs

against an internal standard was performed using the BioNumerics software version 4.5 (Applied Maths, Kortrijk, Belgium). T-RF fragments (range of 60–800 bp) with a difference less than two base pairs were considered identical. Only bands present in both duplicates were accepted as bacterial fragments from which the duplicate with the best intensity was chosen for microbial profiling. The obtained intensities of all T-RFs were imported into Microsoft Excel, and all intensities below 50 were removed. In each sample, the relative intensity of any given selleck chemical T-RF was calculated

by dividing the intensity of the T-RF with the total intensity of all T-RFs in the sample. The most predominant T-RFs with a mean relative intensity above one percent were selected for all further analyses and procedures (except calculation of the diversity and similarity) and their identity was predicted in silico, performed in the MiCA on-line software [24] and Ribosomal Database Project Classifier (322.864 Good Quality, >1200) [25]. T-RFLP statistical analysis All T-RFs between 60 and 800 bp were imported into the statistical software programs Stata 11.0 (StataCorp, College Station, TX), Unscrambler version 9.8 (CAMO, Fludarabine Oslo, Norway) and Microsoft Excel sheets were used for further analyses. Principal component analysis (PCA) was used to explore group differences in the overall microbial communities both for comparisons between cloned pigs and non-cloned controls at the different sampling points and to investigate if samples from pigs with the largest weight-gain during the study period clustered together, irrespective of their genetic background. The latter was also investigated by relating the whole microbial community to the weight-gain at the different sampling points, involving all predominant T-RFs simultaneously in the models.

: Enterotypes of the human gut microbiome. Nature 2011, 473:174–180.PubMedCrossRef 7. Visick KL, Foster J, Doino J, McFall-Ngai M, Ruby EG: Vibrio Fischeri lux genes play an important role in colonization and the development of the host light organ. J Bacteriol 2000, 182:4578–4586.PubMedCrossRef 8. Douglas AE: Mycetocyte symbiosis in insects. Biol Rev Camb Philos Soc 1989, 64:409–34.PubMedCrossRef 9. Hayman DS: Mycorrhizae of nitrogen-fixing legumes. World J Microbiol Biotech 1986, 2:121–145.CrossRef 10. Long

click here SR: Rhizobium symbiosis: nod factors in perspective. Plant Cell 1996, 8:1885–1898.PubMed 11. O’Toole G, Kaplan HB, Kolter R: Biofilm formation as microbial development. Annu Rev Microbiol

2000, 54:49–79.PubMedCrossRef 12. Waters CM, Bassler check details BL: Quorum sensing: cell-to-Cell communication in Bacteria. Annu Rev Cell Dev Biol 2005, 21:319–46.PubMedCrossRef 13. Williams P: Quorum sensing, communication and cross-kingdom signalling in the bacterial world. Microbiology 2007, 153:3923–38.PubMedCrossRef 14. Yim G, Wang HH, Davies J: Antibiotics as signalling molecules. Philos Trans R Soc Lond B Biol Sci 2007, 362:1195–2000.PubMedCrossRef 15. Labbate M, Queck SY, Koh KS, Rice SA, Givskov M, Kjelleberg S: Quorum sensing-controlled biofilm development in Serratia liquefaciens MG1. J Bacterioli 2004, 186:692–698.CrossRef 16. Rice SA, Koh KS, Queck SY, Labbate M, Lam KW, Kjelleberg S: Biofilm formation and sloughing in Serratia marcescens are

controlled by quorum sensing and nutrient cues. J Bacteriol 2005, 186:3477–3485.CrossRef 17. Van Houdt R, Givskov M, Michiels CV: Quorum sensing in Serratia. FEMS Microbiol Rev 2007, 31:407–424.PubMedCrossRef 18. Ben-Jacob E, Shmueli H, Shochet O, Tenenbaum A: Adaptive self-organization during growth of bacterial colonies. Physica A 1992, 187:378–424.CrossRef 19. Golding I, Cohen I, Kozlovsky Y, Ben-Jacob E: Studies of sector formation in expanding bacterial Telomerase colonies. Europhys Lett 1999, 48:587–593.CrossRef 20. Rieger T, Neubauer Z, Blahůšková A, Cvrčková F, Markoš A: Bacterial body plans: colony ontogeny in Serratia marcescens. Communicative Integrative Biology 2008, 1:78–87.PubMedCrossRef 21. Markoš A: The ontogeny of Gaia: the role of microorganisms in planetary information network. J theor Biol 1995, 176:175–180.PubMedCrossRef 22. Jefferson K: What drives bacteria to produce a biofilm? FEMS Microbiology Letters 2004, 236:163–173.PubMed 23. Koschwanez JH, Foster KR, Murray AW: Sucrose utilizationin budding yeast as a model for the origin of undifferentiated multicellularity. PLoS Biol 2011, 9:e1001122.PubMedCrossRef 24. Webb JS, Givskov M, Kjelleberg S: Bacterial biofilms. Prokaryotic adventures in multicellularity. Curr Opin Microbiol 2003, 6:578–585.PubMedCrossRef 25.