Measurements of luminal pH in the normal gastrointestinal tract have shown a progressive increase in pH from the duodenum to the terminal ileum, a decrease in the cecum, and then a slow rise along the colon to the rectum [11]. The relatively acidic pH range of 5.8-6.7 in the human proximal colon (cecum, right colon), the principle site of microbial colonization, has been repeatedly reported using various methods of pH analysis [12–15]. Importantly, pH has been found to be markedly increased in the proximal colon after severe insults such as sepsis,

trauma, shock, and inflammatory bowel disease in human [1, 11] as well as in mouse models of physiological stress induced by major surgery [16]. Yet whether changes in luminal pH correspond to changes within

the colon mucosa, the primary site of a colonization and invasion of P. aeruginosa is unknown. C59 wnt concentration As changes in pH in the proximal colon mucosa have the potential to affect the valence state and hence availability of both phosphate and iron to P. aeruginosa during intestinal colonization, the aims of the present study were to examine if pH changes in the proximal colon mucosa develop in mice following surgical injury that affect the ability of oral phosphate supplementation to protect against lethal sepsis due to intestinal P. aeruginosa. Methods Bacterial strains Studies were performed with P. aeruginosa PAO1 BIBF 1120 mouse strains obtained from two laboratories, MPAO1 (B. Iglewski, the original strain used to create the transposon mutant library at the University of Washington), and CorPAO1 (P. Cornelis), as well as with the CorPAO1 derivative mutant ΔPvdD/ΔPchEF. Mouse model of lethal gut-derived sepsis Animal experiments were approved by the Animal Care and Use Committee at the University of Chicago (IACUC protocol 71744). Male C57BL6/HSD mice VX-680 mw weighing 18 to 22 g were used for all experiments. Gut-derived sepsis was modeled by performing a 30% surgical

left lateral hepatectomy with simultaneous injection of 107 CFU P. aeruginosa into cecum of mice pre-fasted 18 hours prior to surgery as previously described [16]. Mice were allowed access to either tap water, or 25 mM potassium phosphate-buffer (PB) pH 7.5, or 25 mM PB pH 6.0 through over the course of the experimental period. Measurement of intestinal mucosal pH Intestinal mucosa (overlying mucus and triclocarban intestinal epithelial cells) pH was measured with phenol red. Following 24 hrs after surgery, mice were sacrificed, and distal intestine of mice was harvested from rectum to jejunum, gently washed with water to remove loose luminal contents and then stained by flashing 5 times with 0.4% phenol red in buffer (0.145 M NaCl, 0.002 M KH2PO4, 0.003 M Na2HPO4). The intestine was opened longitudinally and mucosal pH measured semi-quantitatively using pH standards stained with phenol red. C. elegans model C. elegans killing assays were performed as we previously reported [9] with modifications. Briefly, P.

In each PFT�� supplier instance, motesanib was a more potent inhibitor of Kit autophosphorylation than imatinib. For example, motesanib inhibited the AYins503-504 mutant with an IC50 of 18 nM, whereas imatinib inhibited this mutant with an IC50 of 84 nM. Interestingly,

the IC50 values for inhibition of these Kit mutants were lower than the IC50 for inhibition of wild-type Kit by motesanib. Consistent results were obtained in a functional viability assay utilizing IL-3-independent growth of Ba/F3 cells (Figure 3C). For example, when testing the AYins503-504 mutant, the IC50 for motesanib was 11 nM versus 47 nM for imatinib. Table 2 Inhibition of the Activity of Wild-Type Kit and Primary Activating Kit Mutants by Motesanib and Imatinib*   IC50 of Kit Autophosphorylation, nM IC50 of Stably Transfected Ba/F3 Cell Survival, nM KIT Genotype Motesanib Imatinib Motesanib Imatinib Wild-type 36 165 – - V560D 5 18 3 7 Δ552-559 1 5 0.4 1 AYins503-504 18 84 11 47 *In autophosphorylation experiments, means from 2 experiments are shown, with the exception of Δ552-559, which was assessed once. Viability experiments were performed once. Figure 3 Inhibition of the activity of wild-type Kit and primary activating Kit mutants by motesanib. Autophosphorylation (expressed

as a percentage of vehicle control) of wild-type Kit (panel A) and primary activating Kit mutants (panel B) was assessed in Talazoparib in vitro stably transfected Chinese hamster ovary cells treated for 2 hours with GDC-0449 in vitro single 10-fold serial dilutions of motesanib. Representative data from 1 of 2 experiments are shown. Viability (expressed as the percentage of vehicle control) of Ba/F3 cells expressing the same primary activating Kit mutants treated

for 24 hours with single 10-fold serial dilutions of motesanib was also assessed (panel C). Viability experiments were Y-27632 2HCl performed once (representative curves are shown). Activity of Motesanib against Imatinib-Resistant Kit Mutants Motesanib inhibited the activity of Kit mutants associated with secondary imatinib resistance. In Kit autophosphorylation assays, motesanib inhibited tyrosine phosphorylation of the juxtamembrane domain/kinase domain I double mutants V560D/V654A and V560D/T670I with IC50 values of 77 nM and 277 nM, respectively. Imatinib had limited activity against the V560D/V654A mutant and no activity against the V560D/T670I mutant at concentrations of up to 3000 nM (Table 3; Figure 4B). Consistent results were obtained in the Ba/F3 cells expressing the V560D/V654A and V560D/T670I mutants with motesanib IC50 values of 91 nM and 180 nM, respectively. Again, motesanib was a more potent inhibitor of these mutants than imatinib (Table 3; Figure 4C).

Our approach, which crosslinks the antibody to the surface-exposed SPA, shows not only a better uptake of the targeted bacteria by the tumor (already 24 h post

intravenous injection), but is also more versatile, since it requires only a specific antibody against a cell surface-exposed ligand to specifically target the bacteria to the ligand-producing cells. Whether these bacteria will be subsequently internalized by the target cells will presumably depend on the cell receptor recognized by the antibody. A769662 Conclusions Certainly, further studies are needed to test this promising cell targeting technology for possible therapeutic applications (e.g. drug delivery to selected cells) but the experiments shown here successfully demonstrate the proof of principle of the approach. Methods Ethics Statement All animals experiments were carried out in accordance with protocols approved by the Regierung von Unterfranken, Germany. Bacterial strains, plasmids, media and growth conditions All strains and plasmids used are listed in Table 1. E.coli DH10b was used for all plasmid DNA manipulations. Competent Lm cells were Selleckchem SAHA HDAC prepared and transformed by electroporation as described by Park and Stewart [30]. All experiments were performed with Lm grown to mid-logarithmic growth phase (OD600 =

0.8) at 37°C cultivated in brain heart infusion (BHI, BD Difco, USA). In experiments indicated, addition of amberlite XAD-4 to the BHI media led to the upregulation of SPA expression Olopatadine in mid-logarithmic phase by activating PrfA and thus listeriolysin promoter P hly . Bacteria were washed twice in 0.9% NaCl (Applichem, Germany) solution, resuspended in 20% v/v glycerol (Applichem, Germany) in 0.9% NaCl solution and stored as aliquots at -80°C. Bacterial

CFUs were determined by plating serial dilutions on BHI agar plates supplemented with 5 μg/ml tetracycline (Sigma, Germany). Table 1 Bacterial strains and plasmids Strains and plasmids Relevant genotype Reference or source L. monocytogenes EGD-e ΔtrpS × pFlo-trpS wild-type T. Chakraborty (PS-341 in vitro University of Giessen, Germany [36] ΔtrpS,inlA/B × pFlo-trpS   [32] Lm-spa- ΔtrpS,aroA,inlA/B × pFlo-trpS This work Lm-spa+ ΔtrpS,aroA,inlA/B,int::Phly-spa × pFlo-trpS This work ΔtrpS × pSP0-PactA-gfp   [36] Lm-spa- × pSP0-P actA -gfp ΔtrpS,aroA,inlA/B × pSP0-PactA-gfp This work Lm-spa+,aroA+ × pSP0-P actA -gfp ΔtrpS,inlA/B,int::Phly-spa × pSP0-PactA-gfp This work Lm-spa+ × pSP0-P actA -gfp ΔtrpS,aroA,inlA/B,int::Phly-spa × pSP0-PactA-gfp This work Plasmids pFlo-trpS TcR, [36] pSP0-PactA-gfp EmR, gfp-ORF, actA-promoter [36] pLSV101intAB EmR, ORIts, mutagenesis plasmid [31] pLSV101intAB::P hly -spa spa-ORF, hly-promoter This work Plasmid and strain construction To amplify the spa gene from S.

Development 1997, 124:3221–3232.PubMed 14. McWhirter JR, Neuteboom ST, Wancewicz EV, Monia BP, Downing JR, Murre C: Oncogenic homeodomain transcription factor E2A-Pbx1 activates a novel WNT gene in pre-B acute lymphoblastoid leukemia. Proc Natl Acad Sci USA 1999, 96:11464–11469.PubMedCrossRef LEE011 chemical structure 15. Smith KS, Chanda SK, Lingbeek M, Ross DT, Botstein D, van Lohuizen M, Cleary ML: Bmi-1 regulation of INK4A-ARF is a downstream requirement for transformation of hematopoietic progenitors by E2a-Pbx1. Mol Cell 2003, 12:393–400.PubMedCrossRef 16. Mounawar M, Mukeria A, Le Calvez F, Hung RJ, Renard H, Cortot A, Bollart C, Zaridze D, Brennan P, Boffetta P: Patterns of EGFR, HER2, TP53, and KRAS mutations

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Among the up-regulated genes in the “translation” category included 50S ribosomal protein L1 (rplA), L20 (rplT), 30S ribosomal protein S2 (rpsB), and translation initiation factor IF-1 (infA) (Additional file 1). Since Ery targets 50S ribosomal proteins and block the ribosome elongation tunnel, this finding suggests that C. jejuni increases transcription of these genes in order to help recover the halted peptide elongation and resume translation as its immediate response against the antibiotic exposure. In the “Defense mechanism” category,

two genes were up-regulated after inhibitory treatment, which encode putative MATE family transport protein (cj0619) buy ARN-509 and ABC-type transmembrane transport protein (cj0607). The role of these genes in the adaptation to Ery treatment remains undetermined. The “cell motility” category comprised the largest proportion of up-regulated genes in response to an inhibitory dose of Ery in wild-type C. jejuni (Table 1), suggesting that enhanced motility might be Campylobacter’s initial escape response to this noxious stress. cj0061c, which encodes the σ28 transcription factor fliA and is essential for normal flagellar

biosynthesis [25], is up-regulated in NCTC 11168 when treated with inhibitory and sub-inhibitory doses of Ery (Table 3). This gene induction was independently confirmed by qRT-PCR (Table LGK-974 chemical structure 4). Previous research indicated that σ28 regulates the major flagellin gene (flaA) and other late genes of the flagellar regulon as well as some non-flagellar genes in C. jejuni[26]. Also, it has been demonstrated that the flaA promoter can be activated by the intestinal environment and C. jejuni chemotactic

effectors, such as bovine bile, deoxycholate, L-fucose, osmolarity, Adenosine aspartate, glutamate, organic acids citrate, fumarate, α-ketoglutarate and succinate [27]. The microarray and qRT-PCR results presented here revealed that Ery induced expression of this regulatory gene (fliA), which might explain why multiple motility genes were up-regulated in C. jejuni under Ery treatment. Compared with the inhibitory-dose Ery treatment, sub-inhibitory dose Ery triggered a much smaller response in the Torin 2 mouse overall transcription in C. jejuni (Table 2 and Additional file 1). There were no or limited changes in most COG categories, except for “poorly characterized” and “amino acid transport and metabolism”. For example, no differentially expressed genes were found in the “energy production and conversion” category under sub-inhibitory Ery treatment (Table 2), while a large portion of genes in this category were down-regulated under the treatment of an inhibitory does of Ery (Table 1).

J Appl Microbiol 2012,113(2):318–328.PubMedCrossRef 40. Riley MA, Wertz JE: Bacteriocins: evolution, ecology, and application. Annu Rev Microbiol 2002,56(1):117–137.PubMedCrossRef 41. Bromberg R, Moreno I, Delboni RR, Cintra HC, Oliveira PTV: Characteristics of the bacteriocin produced by Lactococcus Selleck Sotrastaurin lactis subsp. cremoris CTC 204 and the effect of this compound on the mesophilic bacteria associated with raw beef. World J Microbiol Biotechnol

2005,21(3):351–358.CrossRef 42. de Martinis ECP, Santarosa PR, Freitas FZ: Caracterização preliminar de bacteriocinas produzidas por seis cepas de bactérias láticas isoladas de produtos cárneos embalados a vácuo. Cien Tecnol Alim 2003,23(2):195–199.CrossRef 43. Lewus CB, Sun S, Montville TJ: Production of an amylase-sensitive bacteriocin by an atypical Leuconostoc paramesenteroides strain. Appl Environ Microbiol 1992,58(1):143–149.PubMedCentralPubMed 44. Todorov SD, Dicks LMT: Effect of modified MRS medium on production and purification of antimicrobial peptide ST4SA produced by Enterococcus mundtii . Anaerobe 2009,15(3):65–73.PubMedCrossRef 45. Campos CA, Rodríguez Ó, Calo-Mata P, Prado M, Barros-Velázquez J: Preliminary characterization of bacteriocins from Lactococcus lactis , Enterococcus faecium and Enterococcus mundtii strains

isolated from turbot ( Psetta maxima ). Food Res Int 2006,39(3):356–364.CrossRef 46. Giraffa G, Neviani E: DNA-based, culture-independent strategies for evaluating microbial communities in food-associated ecosystems. Napabucasin Int J Food Microbiol 2001,67(1):19–34.PubMedCrossRef 47. Mohania D, Nagpal R, Kumar M, Bhardwaj A, Yadav M, Jain S, Marotta F, Singh V, Parkash O, Yadav H: Molecular approaches for identification and characterization of lactic acid bacteria. J Digest Dis 2008,9(4):190–198.CrossRef 48. Moraes PM, Perin LM, Silva A Jr, Nero LA: Comparison of phenotypic

and molecular tests to identify lactic acid bacteria. Braz J Microbiol 2013,44(1):109–112.PubMedCrossRef 49. Alegría Á, Delgado S, Roces C, López B, Mayo B: Bacteriocins produced by wild Lactococcus lactis strains isolated from traditional, starter-free cheeses made of raw milk. Int J Food Microbiol 2010,143(1):61–66.PubMedCrossRef 50. Gevers D, Huys G, Swings J: Applicability of rep-PCR fingerprinting for identification of Lactobacillus species. FEMS Microbiol Lett 2001,205(1):31–36.PubMedCrossRef why 51. Mohammed M, Abd El-Aziz H, Omran N, Anwar S, Awad S, El-Soda M: Rep-PCR characterization and biochemical selection of lactic acid bacteria isolated from the Delta area of Egypt. Int J Food Microbiol 2009,128(3):417–423.PubMedCrossRef 52. McAuliffe O, Ryan MP, Ross P, Hill C, Breeuwer P, Abee T: Lacticin 3147, a broad-spectrum bacteriocin which selectively dissipates the membrane potential. Appl Environ Microbiol 1998,64(2):439–445.PubMedCentralPubMed 53. Javed A, Masud T, Ul Ain Q, Imran M, GW-572016 manufacturer Maqsood S: Enterocins of Enterococcus faecium , emerging natural food preservatives.

J Appl Phys 2009,106(2):026104.CrossRef 36. Polman A, Jacobson DC, Eaglesham DJ, Kistler RC, Poate JM: Optical doping of waveguide materials by MeV Er implantation. J Appl Phys 1991,70(7):3778.CrossRef 37. Sckerl MW, Guldberg-Kjaer S, Rysholt Poulsen M, Shi P, Chevallier J: Precipitate coarsening and self organization in erbium-doped silica. Phys Rev B 1999,59(21):13494.CrossRef 38. Crowe IF, Kashtiban RJ, Sherliker B, Bangert U, Halsall MP,

Knights AP, Gwilliam RM: Spatially #Belinostat randurls[1|1|,|CHEM1|]# correlated erbium and Si nanocrystals in coimplanted SiO2 after a single high temperature anneal. J Appl Phys 2010,107(4):044316.CrossRef 39. Lu YW, Julsgaard B, Petersen MC, Jensen RVS, Pedersen TG, Pedersen K, Larsen AN: Erbium diffusion in silicon dioxide. Appl Phys Lett 2010,97(14):141903.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions ET and RL carried out the APT sample preparation by SEM-FIB and performed the atom probe analysis and data treatment. ET, LK, and FG wrote the paper. FG, LK, and KH fabricated the sample under investigation and carried out the optical measurements. PP supervised the study and made significant contributions to the structural properties. All authors read and approved the final manuscript.”
“Background Rare-earth

elements are important optical activators for high throughput screening assay luminescent devices. Among various rare-earth luminescent centers, trivalent praseodymium (Pr3+) offers simultaneously a strong emission in the blue, green, orange, and red spectral range, satisfying the complementary color relationship [1, 2]. Consequently, Pr3+-doped glass/crystals are often used as phosphor materials [2, 3]. SiO2-(Ca, Zn)TiO3:Pr3+ phosphors prepared with nanosized silica particles exhibit an intense red photoluminescence (PL) [3]. The Pr3+ emission was achieved for Si-rich SiO2 (SRSO) implanted with Pr3+ ions, but its intensity Resminostat was lower

[4]. Hafnium dioxide (HfO2) and hafnium silicates (HfSiO x ) are currently considered as the predominant high-k dielectric candidates to replace the conventional SiO2 due to the rapid downscaling of the complementary metal-oxide semiconductor (CMOS) transistors [5, 6]. It is ascribable to their good thermal stability in contact with Si, large electronic bandgaps, reasonable conduction band offset in regard to Si, and their compatibility with the current CMOS technology. Our group has first explored the structural and thermal stability of HfO2-based layers fabricated by radio frequency (RF) magnetron sputtering [7, 8] and their nonvolatile memory application [9, 10]. It is worth to note that both HfO2 and HfSiO x matrices have lower phonon frequencies compared to those of SiO2, and as a consequence, both are expected to be suitable hosts for rare-earth activators.

In a typical SERS measurement protocol, 2.5 μL of an check details R6G solution in ethanol 80 μM in concentration was Selleck MAPK inhibitor applied onto the surface of the substrate under study. The average surface area occupied by the dye droplet spread on the substrate was around 7 mm2. Measurements were mainly taken using radiation from a He-Ne laser (wavelength 632.8 nm, power in the beam spot approximately 5 mW). The laser beam spot diameter was around

20 μm, and the signal accumulation time came to 10 s (the signal was averaged over 10 measurements). With the test conditions remaining the same, SERS signals were measured from the R6G dye applied onto GNR-Si and GNR-OPC substrates differing in thickness of the opal-like film. Figure 5 shows the SERS spectra of the 80 μM rhodamine 6G solution applied onto a GNR-Si (spectrum 1) and a GNR-OPC (spectrum 2) substrate excited at 632.8 nm. Evidently, the integral analytical enhancement [42] of the GNR-OPC substrate is from two to five times as high as that of the simple fractal-like GNR assembly

on silicon. A common property of SERS measurements is that the integral enhancement depends on the particular Raman line selected for the purpose. The fundamental Selleckchem Fludarabine SERS enhancement [41, 42] is determined by several important factors that are difficult to take into account for mesoporous substrates. For a detailed discussion of this point, the readers are referred to the comprehensive analysis by Le Ru et al. [36]. Figure 5 SERS spectra of 80

μM rhodamine 6G solution applied onto GNR-Si (1) and thin GNR-OPC (2) substrates. Excited at 632.8 nm. In Figure 6, we compare between the SERS spectra of the 80 μM rhodamine 6G solution applied onto ‘thin’ and ‘thick’ GNR-OPC substrates. This classification roughly corresponds to the number of the deposited silica layers, which is less than 10 in the former case and more than 10 in the latter. However, in both cases, the pores between silica spheres are densely covered by GNRs, but GNRs fail these to cover the silica spheres completely. Surprisingly enough, the maximum SERS enhancement is observed with thin rather than thick substrates (cf. spectra 1 and 2 in Figure 6). It should be noted that the elevated tail in SERS spectrum 2 is due exactly to a thick silica film contribution. For thin substrates, the baseline is flat (similar to that for spectrum 1 in Figure 6). Moreover, for extremely thick substrates (about 1 to 2 mm thick), the SERS enhancement falls down, and we observe a monotonous contribution from the underlying silica opal (data not shown). Figure 6 SERS spectra of 80 μM rhodamine 6G solution applied onto thin (1) and thick (2) GNR-OPC substrates. Excited at 632.8 nm. Taking into account the analytical SERS enhancement coefficient of GNR-Si substrates [33] (2.5 × 103), we estimate the analytical enhancement coefficient of GNR-OPC substrates to be on the order of 104. We suppose that the additional SERS enhancement in the GNR-OPC substrates is due to several factors.

Biochim Biophys Acta 546(1):121–141PubMed Kirchhoff H, Tremmel I, Haase W, Kubitscheck U (2004) Supramolecular photosystem II organization in grana thylakoid membranes: evidence for a structured arrangement. Biochemistry 43(28):9204–9213PubMed Kirchhoff H, Haferkamp S, Allen JF, Epstein DBA, Mullineaux

CW (2008a) Protein diffusion and macromolecular crowding in thylakoid membranes. Plant Physiol 146(4):1571–1578PubMed Kirchhoff H, Lenhert S, Büchel C, Chi L, Nield J (2008b) Probing the organization of photosystem II in photosynthetic membranes by atomic force learn more microscopy. Biochemistry 47(1):431–440PubMed Kiss AZ, Ruban AV, Horton P (2008) The PsbS protein controls the organization of the photosystem II antenna in higher plant thylakoid membranes. J Biol Chem 283(7):3972–3978PubMed Duvelisib Kouřil R, Oostergetel GT, Boekema EJ (2011) Fine structure of granal thylakoid membrane organization CH5183284 using cryo electron tomography. Biochim Biophys Acta 1807(3):368–374PubMed Kouřil R, Wientjes E, Bultema JB, Croce R, Boekema EJ (2012a) High-light vs. low-light: effect of light acclimation on photosystem II composition

and organization in Arabidopsis thaliana. Biochim Biophys Acta 1827(3):411–419 Kouřil R, Dekker JP, Boekema EJ (2012b) Supramolecular organization of photosystem II in green plants. Biochim Biophys Acta 1817(1):2–12PubMed Krause GH (1973) The high-energy state of the thylakoid system

as indicated by chlorophyll fluorescence and chloroplast shrinkage. Biochim Biophys Acta 292(3):715–728PubMed Krause G, Weis E (1991) Chlorophyll fluorescence and photosynthesis: the basics. Annu Rev Plant Biol 42(1):313–349 Kulheim C, Agren J, Jansson S (2002) Rapid regulation of light harvesting and plant fitness in the field. Science 297(5578):91–93PubMed Teicoplanin Lakowicz JR (2006) Principles of fluorescence spectroscopy, 3rd edn. Springer, New York Li XP, Bjorkman O, Shih C, Grossman AR, Rosenquist M, Jansson S, Niyogi KK (2000) A pigment-binding protein essential for regulation of photosynthetic light harvesting. Nature 403(6768):391–395PubMed Li XP, Muller-Moule P, Gilmore AM, Niyogi KK (2002a) PsbS-dependent enhancement of feedback de-excitation protects photosystem II from photoinhibition. Proc Natl Acad Sci USA 99(23):15222–15227PubMed Li XP, Phippard A, Pasari J, Niyogi KK (2002b) Structure–function analysis of photosystem II subunit S (PsbS) in vivo. Funct Plant Biol 29(10):1131–1139 Liu LN, Sturgis JN, Scheuring S (2011) Native architecture of the photosynthetic membrane from Rhodobacter veldkampii. J Struct Biol 173(1):138–145PubMed Ma YZ, Holt NE, Li XP, Niyogi KK, Fleming GR (2003) Evidence for direct carotenoid involvement in the regulation of photosynthetic light harvesting.

However, no significant change was shown in the abundance of genes involved in recalcitrant C (e.g., lignin) degradation. Therefore, our results indicate that eCO2 significantly affected metabolic potentials for C fixation and degradation. However, it appears that such changes have little effect on soil C storage [25], probably due to accelerated degradation of increased C inputs, which is consistent with increased soil CO2 flux over the course of the experiment. Another important question is click here YH25448 solubility dmso whether eCO2 affects soil N cycling processes and/or

soil N dynamics. Our previous study has showed that soil N supply is probably an important constraint on global terrestrial productivity in response to eCO2[32]. When N is limiting, decomposers may respond to increased C inputs by decomposing soil organic matter to gain access to N and constrain the plant biomass accumulation at eCO2[42, 43]. In this study, our GeoChip analysis showed that the abundance of nifH genes significantly increased at eCO2. Presumably, an increase

in N2 fixation under eCO2 may lead to enhanced CO2 fertilization of plant biomass production by alleviating some of the N constraints on plant response to eCO2. In the plots examined in the present selleck inhibitor study, no N fertilizer was supplemented, but significant increases were observed in the total plant biomass and aboveground plant biomass, especially the biomass of legume plant species Lupinus perennis, which may be associated with significant increases of N2 fixers in soil under eCO2 measured by the abundance of nifH genes in this study. At eCO2, if the increased nifH abundance is interpreted as potential increase of soil microbial N2 fixation, such increase could supplement N nutrients for the plant growth to eliminate the N limitation constraint. In addition, the abundance of until nirS genes significantly increased at eCO2 while all others genes involved in denitrification

remained unaffected. The results suggest that eCO2 could significantly impact microbial N2 fixation and denitrification, and probably enhance the production of the greenhouse gas N2O. However, it appears that no significant changes were observed in soil N dynamics under eCO2, which may be largely due to the large N pool size in soil. It is largely unknown whether or how eCO2 and eCO2-induced effects, such as increased C inputs into soil and changes in soil properties, shape soil microbial community structure. The direct effects of elevated atmospheric CO2 concentration on soil microbial communities were expected to be negligible compared to potential indirect effects such as increased plant C inputs to soil, since the CO2 concentrations in the pore space of soil generally is much higher than those in the atmosphere even under ambient CO2 concentrations [5]. However, this has not been well studied.