Int J Parasitol 28:776–786CrossRef Adrianov AV (2004) Current problems in marine biodiversity studies. Russ J Mar Biol 30(1):1–16CrossRef Selleckchem GSK2118436 Blaxter M (2008) TardiBASE—the home of the Edinburg Tardigrade Project. http://​xyala.​cap.​ed.​ac.​uk/​tardigrades/​tardibase.​html. Accessed 26 June 2009 Cesari M, Bertolani R, Rebecchi L, Guidetti R (2009) DNA barcoding in Tardigrada: the first case study on Macrobiotus macrocalix Bertolani & Rebecchi 1993 (Eutardigrada, Macrobiotidae). Mol Ecol Resour 9:699–706CrossRef

Commission of the European Communities (2006) Halting the loss of biodiversity by 2010—and ACP-196 beyond; sustaining ecosystem services for human well-being. Commission of the European Communities, Brussels Convention on https://www.selleckchem.com/products/Trichostatin-A.html Biological Diversity (2001) 2010 Biodiversity target. http://​www.​biodiv.​org/​2010-target/​default.​asp.

Accessed 15 July 2009 Faurby S, Jönson KI, Rebecchi L, Funch P (2008) Variation in anhydrobiotic survival of two eutardigrade morphospecies: a story of cryptic species and their dispersal. J Zool 275:139–145CrossRef Guidetti R, Schill R, Bertolani R, Dandekar T, Wolf M (2009a) New molecular data for tardigrade phylogeny, with the erection of Paramacrobiotus gen. nov. J Zool Syst Evol Res 47(4):315–321CrossRef Guidetti R, Rebecchi L, Bertolani R, Cesari M, Jorgensen A (2009b) Tardigrada barcoding—TABAR. http://​www.​barcodinglife.​org. Accessed 20 October 2009 Guil N, Sánchez-Moreno S, Machordom A (2009) Local biodiversity patterns in micrometazoans: are tardigrades everywhere? Syst Biodivers 7(3):259–268CrossRef Gyedu-Ababio TK, Furstenberg JP, Baird D, Vanreusel A (1999) Nematodes as indicators of pollution: a case study from the Swartkops River system, South Africa. Hydrobiologia 397:155–169CrossRef Horikawa DD, Higashi S (2004) Desiccation Cyclic nucleotide phosphodiesterase tolerance of the tardigrade Milnesium tardigradum collected in Sapporo, Japan, and Bogor, Indonesia. Zool Sci 21:813–816CrossRefPubMed Jovan S (2008) Lichen bioindication of biodiversity, air quality, and climate: baseline results from monitoring

in Washington, Oregon, and California. Gen. Tech. Rep. PNW-GTR-737. U.S. Department of Agriculture, Forest Service, Pacific Northwest Research Station, Portland, 115 pp Kinchin IM (1992) An introduction to the invertebrate microfauna associated with mosses and lichens with observations from maritime lichens on the West coast of the British Isles. Microscopy 36:721–731 Kunieda T, Katayama T, Toyoda A, Horikawa D, Arakawa K, Kuwahara H, Yamaguchi A, Aizu T, Abe W (2008) Kumamushi Genome Project. http://​kumamushi.​org. Accessed 20 July 2009 Lévêque C, Balian EV, Martens K (2005) An assessment of animal species diversity in continental waters. Hydrobiologia 542:39–67CrossRef Malmström A, Person T, Ahlström K, Gongalsky KB, Bengtsson J (2009) Dynamics of soil meso- and macrofauna during a 5-year period after clear-cutburning in a boreal forest.

Q. aquatica K.D. Hyde & Goh, Q. microsporum Yin. Zhang, K.D. Hyde & J. Fourn. and Q. submerse K.D. Hyde & Goh, which are all from freshwater (Hyde and Goh 1999; Zhang et al. 2008b). Phylogenetic

study Multigene phylogenetic study indicated that Quintaria lignatilis forms a separate sister clade to other families of Pleosporales, which may represent a new familial linage (Suetrong et al. 2009). This was supported by phylogenetic studies which place the freshwater Q. submersa separate from Q. lignatilis (Schoch et al. 2009; Suetrong et al. 2009; Plate 1). Concluding remarks The freshwater members of Quintaria should likely be excluded Akt inhibitor from this genus, and only the generic type, Q. lignatilis www.selleckchem.com/products/th-302.html retained, but this needs confirmation. Roussoëlla Sacc., in Saccardo & Paoletti, Atti Inst. Veneto Sci. lett., ed Arti, Sér. 3 6: 410 (1888). (Arthopyreniaceae (or Massariaceae))

Generic description Habitat terrestrial, saprobic. Ascomata medium-sized, clustered, immersed in host tissue, forming under darkened, slightly raised, somewhat liner or dome-shaped stroma on the host, with a flush intra-epidermal papilla; immersed under clypeus, papillate, ostiolate. Peridium thin, comprising several layers of compressed cells. Hamathecium of dense, long trabeculate pseudoparaphyses, embedded in mucilage, hyaline, anastomosing and septate. Asci 8-spored, bitunicate, cylindrical, with furcate pedicel, and a conspicuous ocular chamber. Ascospores uniseriate to partially overlapping, fusoid or ellipsoidal, selleck screening library brown, 1-septate, constricted at the septum. Anamorphs reported for genus: Cytoplea (Hyde et al. 1996a). Literature: Hyde et al. 1996a; Hyde 1997;

Ju et al. 1996; Tanaka et al. 2009. Type species Roussoëlla nitidula Sacc. & Paol., Atti Ist. Veneto Sci., Ser. 6, 6:410. (1888). (Fig. 83) Fig. 83 Roussoëlla nitidula (from PAD Paol. 2484, holotype). a Appearance of the stroma on host surface. b Asci and pseudoparaphyses. c, d Long cylindrical furcate asci. E-H. Ascospores. Note the striate ornamentation. Scale bars: a = 0.5 mm, b–d = 20 μm, e–h = 10 μm Ascomata 160–200 μm high × 400–500 μm diam., clustered, immersed in host tissue, forming under darkened, slightly raised, somewhat liner or dome-shaped stroma on the host, with a flush intra-epidermal papilla; in vertical section subglobose with a flattened base, immersed under clypeus, subglobose with a flattened base, papillate, BIBW2992 cost ostiolate (Fig. 83a). Peridium up to 20 μm thick, comprising several layers of compressed cells. Hamathecium of dense, long trabeculate pseudoparaphyses, 1–1.5 μm broad, embedded in mucilage, anastomosing and septate. Asci 123–220 × 7–11 μm, 8-spored, bitunicate, cylindrical, with furcate pedicels, and a conspicuous ocular chamber (Fig. 83b, c and d). Ascospores 17.5–22 × 5.

The frequency of phylum Firmicutes was major in tumor tissues (85%) as compared to check details non-tumor tissues (74.6%) whereas the frequency of other phyla was higher in non-tumor library. The composition of bacterial communities at tumor site was different in comparison to the non-tumor site in most of the patients (Figure 4a). In combined library, 12 classes, 16 order, 26 families and 40 genera were observed and their relative

distribution in individual non-tumor and tumor library is demonstrated in (see Additional file 1: Figure S1, Additional file 2: Figure S2, Additional file 3: Figure S3) and Figure 4b respectively. The most prevalent classes were Bacilli (66.6%) that includes order, Lactobacillales (54.8%) and Bacillales (11.8%) in tumor library while Clostridia (20.5%) and Bacteroides (11.8%) in non-tumor library. SN-38 order Figure 3 Distribution of relative abundance of phyla in (a) Individual EPZ015938 nmr sample set, non-tumor and tumor sites

of each OSCC patient and; (b) Cumulative non-tumor and tumor libraries, as detected by HOMD and RDP. N–Non-tumor; T–Tumor. Figure 4 Distribution of relative abundance of genera at (a) Non-tumor and tumor sites of each OSCC subject; and (b) Cumulative non-tumor and tumor libraries, as detected by HOMD and RDP; (c) Pie-chart shows the relative prevalence of gram-negative and gram-positive bacteria and venn diagram depicts the genera in tissue samples of OSCC subjects. *p < 0.1. N–Non-tumor; T–Tumor. Pie-chart shows the relative shift of gram-negative and gram-positive microbiota in non-tumor and tumor tissue samples. Values in the venn diagram represent the genera shared by and exclusive to non-tumor and tumor tissue libraries. The distribution Mirabegron of relative abundance of 40 representative genera in combined library (Figure 4b) was predominated by Streptococcus (50.8%), Gemella (11.6%), Parvimonas (4.6%), Peptostreptococcus (2.8%), Xanthomonas (2.4%), Johnsonella (1.6%), Solobacterium (1.6%), Atopobium (1.2%) and Eubacterium[[11]][G-1] (0.8%), in tumor library while Prevotella (11.6%), Veillonella

(9.9%), Granulicatella (3.9%), Escherichia coli (2.4%), Oribacterium (2.2%), Fusobacterium (1.9%), Actinomyces (1.4%), Megasphaera (1.4%), Afipia (1.2%) and Leptotrichia (1.0%) in non-tumor library. Among others, genera Capnocytophaga, Selenomonas and Leptothrix were exclusive to non-tumor (control) tissues and Eubacterium[[11]][G-3], Campylobacter and Catonella, confined only to tumor tissues. Figure 4c shows the relative shift from gram-negative to gram-positive microbiota by an increase of 19% in tumor tissue samples than in control non-tumor samples. Also, it was observed that the two groups shared 25 genera, while 7 genera were exclusive to non-tumor group and 8 genera to tumor group (Figure 4c). The core of pie chart shows % distribution of 914 total sequences in terms of % homology to curated 16S rRNA sequences in HOMD (Figure 5).

J Phys Chem C 2009, 113:14071–14075.

10.1021/jp906348xCrossRef 24. Salihoglu O, Balci S, Kocabas C: Plasmon-polaritons on graphene-metal surface and their use in biosensors. Appl Phys Lett 2012, 100:213110. 10.1063/1.4721453CrossRef 25. Jung JH, Cheon DS, Liu F, Lee KB, Seo TS: A Go6983 Graphene oxide based immuno-biosensor for pathogen detection. Angew Chem Int Ed 2010, 49:5708–5711. 10.1002/anie.201001428CrossRef 26. Liu J, Fu S, Yuan B, Li Y, Deng Z: Toward a universal “adhesive nanosheet” for the assembly of multiple nanoparticles based on a protein-induced reduction/decoration of graphene oxide. J Am Chem Soc 2010, 132:7279–7281. 10.1021/ja100938rCrossRef 27. Guo S, Dong S: Graphene and its derivative-based sensing materials for analytical devices. J Mater Chem 2011, 21:18503–18516. 10.1039/c1jm13228hCrossRef AZD6738 order this website 28. Mohanty N, Berry V: Graphene-based single-bacterium resolution biodevice and DNA transistor: interfacing graphene derivatives with nanoscale and microscale biocomponents. Nano Lett 2008, 8:4469–4476. 10.1021/nl802412nCrossRef 29. Shin SY, Kim

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Colloids Surf B: Biointerfaces 2010, 81:508–512. 10.1016/j.colsurfb.2010.07.049CrossRef 33. Georgakilas V, Otyepka M, Bourlinos AB, Chandra V, Kim N, Kemp KC, Hobza P, Zboril R, Kim KS: Functionalization of graphene: covalent and non-covalent approaches, derivatives and applications. Chem Rev 2012, 112:6156–6214. 10.1021/cr3000412CrossRef 34. Chen D, Feng H, Li J: Graphene oxide: preparation, functionalization, and electrochemical applications. Chem Rev 2012, 112:6027–6053. 10.1021/cr300115gCrossRef 35. Bai H, Li C, Shi G: Functional composite materials based on chemically converted graphene. Adv Mater 2011, 23:1089–1115. 10.1002/adma.201003753CrossRef 36. Tu Q, Pang L, Chen Y, Zhang Y, Zhang R, Lu B, Wang J: Effects of surface charges of graphene oxide on neuronal outgrowth and branching. Analyst 2014, 139:105–115. 10.1039/c3an01796fCrossRef 37. Katz EY: A chemically modified electrode capable of a spontaneous immobilization of amino compounds due to its functionalization with succinimidyl groups. J Electroanal Chem 1990, 291:257–260. 10.1016/0022-0728(90)87193-NCrossRef 38.

S. Katsu, Vice-President Mr. M. Mamashev) assisted in meeting the publication costs of this article. References 1. Zhao Y, Zhang Y, Gosselink D, Doan TNL, Sadhu M, Cheang HJ, Chen P: Polymer electrolytes for lithium/sulfur batteries. Membranes 2012, 2:553–564.CrossRef 2. Zhang Y, Zhao Y, Sun KEK, Chen P: Development in lithium/sulfur ��-Nicotinamide mouse secondary batteries. Open Mater Sci J 2011, 5:215–221.CrossRef 3. Yang Y, Zheng G, Cui

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doi:10.1007/s11581-013-1042-7 8. Wang C, Wan W, Chen JT, Zhou HH, Zhang XX, Yuan LX, Huang YH: Dual core-shell structured sulfur cathode composite synthesized by a one-pot route for lithium sulfur batteries. J Mater Chem A 2013, 1:1716–1723.CrossRef 9. Hassoun J, Scrosati B: A high-performance polymer tin sulfur lithium ion battery. Angew Chem Int Ed 2010, 49:2371–2374.CrossRef 10. Zhao Y, Zhang Y, Bakenov Z, Chen P: Electrochemical performance

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The two West African GW2580 chimpanzee subspecies, Pan troglodytes ellioti and Pan troglodytes verus, appear to be free from SIVcpz infection. Therefore it is hypothesized that this virus was introduced after the evolutionary divergence and geographical separation of the West African subspecies from the Central/East subspecies [11, 15]. To test for SIVcpz in P. t. verus, more than 1500 captive chimpanzees of this subspecies have been screened for this Nec-1s concentration virus.

However, these chimpanzees do not represent the wild population since only 447 were wild-born and have mainly been captured as infants, when they are less likely to be infected [15, 19]. Therefore, it remains important to continue to collect data on wild living chimpanzees from this subspecies. To date,

the only study on wild living P. t. verus has been based on 28 faecal samples from a population in Taï National Park, Côte d’Ivoire [16]. The chimpanzees of Taï National Park have been under human observation for more than 30 years [20] and are known to hunt and consume monkeys frequently. When hunting, the chimpanzees bite their prey and are sometimes bitten in return. The prey is consumed almost entirely, which means that many bones are crushed which could cause lesions in the oral cavity and result in direct blood to blood contact. They hunt weekly throughout the year and usually every day in the hunting season from September to November, and 80% of their prey consist of western red colobus monkeys (Piliocolobus www.selleckchem.com/products/MGCD0103(Mocetinostat).html badius badius) [20]. These red colobus monkeys harbour high levels of their own species specific strain of SIV (SIVwrc) as well as two other retroviruses; Simian T-cell Lymphotrophic Virus type 1 (STLV-1wrc) and Simian Foamy Virus (SFVwrc) [21–25]. Based on the SIVwrc prevalence data from this red colobus Molecular motor population (50 to 82% of the population is positive [21]) and based on hunting data from the Taї Chimpanzee Project [20],

we estimate that adult male chimpanzees are yearly exposed to approximately 45 kilograms of SIV infected red colobus tissue. Therefore the chimpanzees are exposed to high levels of SIVwrc through biting, blood-to-blood/mucosa contact and ingestion of their prey. This may provide possible infection routes for the virus, although the modes of SIV transmission are not fully known [7, 8]. It has already been documented that the other two retroviruses harboured by the red colobus monkeys in Taї National Park; STLV-1wrc and SFVwrc, are transmitted to the Taї chimpanzee population (individuals are included in the present study) most likely through hunting and meat consumption [22, 23]. Further, in chimpanzee subspecies where the chimpanzee lentivirus, SIVcpz, has been documented, it is believed that this mosaic virus was initially acquired through hunting and consumption of infected monkey prey species [9–11].

No positive PCR results were obtained in this collection for genes coding for plasmid-mediated AmpC-β-lactamases. The ESBL genes produced by the 19 obtained transconjugants were: bla CTX-M-14 (16/19, 84.2%), bla CTX-M-9 (1/19, 5.3%), bla SHV-12 (1/19, 5.3%) and bla TEM-200 (1/19, 5.3%). Hybridization assays showed that the gene coding for CTX-M-14 was mobilizable by IncK plasmids. Moreover, the RFLP of plasmids from 13 IncK-CTX-M-14 showed the same check details restriction pattern

in 8 isolates (Figure 3) (unfortunately, for the remaining 5 isolates the assay did not allow the production of a restriction pattern). Figure 3 Restriction patterns to the IncK-CTX-M-14-plasmids belong to Androgen Receptor inhibition transconjugants obtained from the ESBL collection.

Amoxicillin resistance https://www.selleckchem.com/products/tubastatin-a.html in the 45 Ec-MRnoB isolates was related to genes coding for TEM-1 (36/45, 80%), SHV-11 (2/45, 4.4%), SHV-1 (1/45, 2.2%) or OXA-1 (1/45, 2.2%). The relationship between amoxicillin resistance and TEM-1 production in these organisms was confirmed by detecting the corresponding gene in 24 out the 25 (96%) obtained transconjugants. The Ec-MRnoB resistant to both extended-spectrum cephalosporins and cefoxitin contained the gene coding for CMY-2, which was included in IncA/C plasmids, as confirmed by hybridization assays. None of the 69 Ec-ESBL or the 45 Ec-MRnoB contained any of the studied plasmid-mediated quinolone resistance genes. In the 69 Ec-ESBL isolates, class 1, class 2 or class 1 plus class 2 integrons were detected in 33.3%, 10.1% and 2.9% isolates, respectively (Table 3). Similarly, for the 45 Ec-MRnoB, positive results for class 1, class 2, and class 1 plus class 2 integrons were obtained for 75.6%, 4.4%, and 6.7% of the isolates (Table 4). The gene cassette arrays found in class 1 integrons for both E. coli collections are shown in Tables 3 and 4. Orotidine 5′-phosphate decarboxylase Table 3 Distribution of gene cassette arrays found in class 1 integrons among phylogenetic groups of E. coli belongs to Ec-ESBL collection     Phylogenetic groups (number of isolates) Cassettes Total A (N=23) B1 (N=26) B2 (N=5) D (N=15) ant(3″ )-Ia 3 2 (8.7%) 0 0 1 (6.7%) dfrA1-ant(3″ )-Ia 7 4 (17.4%) 2 (7.7%)

0 1 (6.7%) bla OXA-1 -ant(3″ )-Ia 1 1 (4.3%) 0 0 0 dfrA12-ant(3″ )-Ib 0 0 0 0 0 dfrA16-ant(3″ )-Ib 4 2 (8.7%) 1 (3.8%) 0 1 (6.7%) dfrA17-ant(3″ )-Ie 8 3 (13%) 1 (3.8%) 1 (20%) 3 (20%) ant(2″ )-Ia 0 0 0 0 0 ant(3″ )-Ia-ant(2 ″ )-Ia 0 0 0 0 0 Table 4 Distribution of gene cassette arrays found in class 1 integrons among phylogenetic groups of E. coli belongs to Ec-MRnoB collection     Phylogenetic groups (number of isolates) Cassettes Total A (N=14) B1 (N=9) B2 (N=7) D (N=15) ant(3″ )-Ia 5 0 3 (33.3%) 1 (14.3%) 1 (6.7%) dfrA1-ant(3″ )-Ia 6 3 (21.4%) 1 (11.1%) 0 2 (13.3%) bla OXA-1 – ant(3″ )-Ia 1 1 (7.1%) 0 0 0 dfrA12 – ant(3″ )-Ib 3 1 (7.1%) 0 1 (14.3%) 1 (6.7%) dfrA16 – ant(3″ )-Ib 0 0 0 0 0 dfrA17 – ant(3″ )-Ie 16 4 (28.6%) 2 (22.2%) 4 (57.

At the univariate analysis, age (p <

0.0001), Okuda stage (p = 0.046) (Figure 5), type of TACE (P < 0,0001) and number of TACE treatments (p = 0.003) were found to be prognostic factors influencing overall survival. Type of TACE (p = 0.0003) and the number of TACE treatments (p = 0.004) were also found to be prognostic factors influencing the time to progression. Figure 5 Median overall survival for Apoptosis Compound Library screening global patients population according to the Okuda staging system: Okuda 1(—), Okuda 2 (———) and Okuda 3 (………)

(33 vs 29 vs 14 months, p = 0.046). CA3 ic50 At multivariate analysis, age, the Okuda stage, type of TACE and number of TACE treatments proved to be independent prognostic factors influencing overall survival (p < 0.0001). Only type and number of TACE treatments proved to be independent prognostic factors influencing time to progression (p < 0.0001). Overall response rate for patients treated with lipiodol TACE or pTACE respectively was: complete response in 17 (20%) and 14 (24%) patients, partial remission ADAMTS5 in 32 (39%) GSK872 solubility dmso and 19

(33%) patients, stable disease in 16 (19%) and 7 (12%) patients, and progressive disease in 18 (22%) and 18 (31%) patients. No statistically significant differences in terms of objective response (assessed according to RECIST criteria) was found between the groups of patients treated with lipiodol TACE or pTACE with microspheres (Table 3). Table 3 Response rate observed in the global case series and according to treatment received (lipiodol TACE or pTACE) (CR = complete remission; PR = partial remission; SD = stable disease; PD = progressive disease NA = not available) Objective response     TACE lipiodol pTACE microspheres Total CR (%) 17 (20) 14 (24) 31 (22) PR (%) 32 (39) 19 (33) 51 (36) SD (%) 16 (19) 7 (12) 23 (15) PD (%) 18 (22) 18 (31) 36 (27) NA 8 1 9 The toxicity profiles (were not statistically different between the groups of patients treated with lipiodol TACE or pTACE (Table 4). Table 4 Main toxicity results for lipiodol TACE and pTACE according to NCI-CTC 3.0 (National Cancer Institute – Common Toxicity Criteria 3.0).

Treatment resulted in a limited increase of calciuria without increase of the prevalence of hypercalciuria. Compared to the 20-µg teriparatide treatment, a treatment with a higher daily dose of 40 µg teriparatide resulted in a click here larger increase of BMD at the lumbar spine and the femoral neck, a larger decrease of BMD at the shaft of the radius, a similar reduction in the risk of vertebral and nonvertebral fracture, and a higher incidence of hypercalcemia [108, 109]. In contrast with the effects of antiresorptive drugs on biochemical markers of bone turnover,

Selleck Cilengitide the treatment effects of teriparatide on BMD and fracture risk reduction are underlied by marked and sustained increases in the biochemical markers of bone turnover, an initial rapid and marked increase of the markers of bone formation being followed with a delay of about 1 month by a less pronounced increase of the markers of bone resorption [110]. The magnitude of

early changes in markers of bone formation has been shown to correlate with increases of BMD at 18 months of treatment [111] and with improvements in bone structure as shown by histomorphometry and including augmentation of cancellous bone with increased trabecular thickness and connectivity [112]. The antifracture efficacy of teriparatide on spinal fracture does not seem to be

modulated by age of the subjects (<65, 65–75, or >75 years), prevalent KPT-8602 molecular weight Acetophenone spinal BMD values (T-score <−2.5 or >−2.5), or the number of prevalent fractures (one or two or more fractures) [113], and the response to treatment does not appear different in postmenopausal patients with baseline 25(OH)D insufficiency (serum 25(OH)D >10 but ≤75 nmol/ml) or sufficiency (>75 nmol/ml) [114]. At the end of the randomized placebo controlled trial having demonstrated the efficacy of 20 µg daily subcutaneous injections of teriparatide in postmenopausal osteoporosis [108], the patients were followed for an additional 18-month period without teriparatide, during which they were allowed to use any antiosteoporotic medication considered appropriate by their treating physician. While the proportion of patients having received an inhibitor of bone resorption was slightly higher in patients previously in the placebo group than in the patients having been treated with 20 µg/day teriparatide, the reduction of vertebral fractures observed in this particular group during the initial trial was confirmed during this 18-month follow-up observation period (RR, 0.59; 95% CI, 0.42–0.85) [115].

2). The annotated genome of S. meliloti 1021 has 54% of genes located in the MK0683 datasheet chromosome, 25% on pSymB and 21% on pSymA. The distribution of tolC-dependently

expressed genes shows a replicon bias with 1.50-fold higher impact on the chromosome encoded transcripts. Contrastingly, genes from pSymB and pSymA were under-represented with 0.65- and 0.14-fold, respectively. Figure 1 Effect of tolC mutation on growth of S. meliloti 1021. Growth curves of S. meliloti 1021 (◊) and SmLM030-2 tolC mutant (■) were obtained in GMS medium. Optical density values are the means of three independent experiments. The arrow indicates the time point where cells were collected for total RNA extraction. Error bars show standard deviations. Asterisks represent data points with significantly different means (p-value < 0.01). Figure 2 Distribution of differentially expressed genes in GSI-IX function of the S. meliloti 1021 replicons. The histogram shows the number of differentially expressed genes obtained when the tolC mutant transcriptome was compared to the wild-type strain and their distribution on the chromosome and the two megaplasmids pSymA and pSymB. A total

of 1177 genes (Table 1 and Additional file 1: Table S1) had significantly increased expression in selleck chemicals the tolC mutant. These could be classified in 20 functional categories. Fig. 3 summarizes the percentages of differentially expressed genes in comparison to genes of the same category represented on the microarray. The largest categories, with more than 30% of the genes with significantly increased expression, included genes involved into protein synthesis, defense, cell motility, protein modification and turnover, energy production,

nucleotide metabolism, 3-oxoacyl-(acyl-carrier-protein) reductase and genes of unknown function (Fig. 3, grey bars). Microarray analysis revealed that expression of 325 genes was significantly decreased in the tolC mutant (Table 2 and Additional file 2: Table S2). Largest categories, with more than 10% of the genes with a significantly decreased expression include the genes involved in cell division, amino acid transport and metabolism, and of unknown function (Fig. 3, black bars). Table 1 Genes with more than 8-fold increased expression in the tolC mutant strain. Gene identifier Annotation or description Fold change1(tolC vs. wild-type) Signal transduction SMb21560 Putative two-component sensor histidine kinase 14.7 SMb21561 Putative two-component response regulator 27.1 Translation SMc00320 rbfA probable ribosome-binding factor A, rRNA processing protein 8.9 SMc00323 rpsO robable 30 S ribosomal protein S15 8.7 SMc00324 pnp probable polyribonucleotide nucleotidyltransferase 10.1 SMc00335 rpsA 30 S ribosomal protein S1 10.2 SMc00485 rpsD probable 30 S ribosomal subunit protein S4 9.2/8.8 SMc00522 rhlE1 putative ATP-dependent RNA helicase 8.5 SMc00565 rplI probable 50 S ribosomal protein L9 13.4 SMc00567 rpsR putative 30 S ribosomal protein S18 21.9 SMc00568 rpsF putative 30 S ribosomal protein S6 25.