, 2011). YeeV inhibits the cell division by blocking the polymerization of FtsZ and MreB. We thus examined whether YgfX also interferes with FtsZ and MreB functions. In order to assess the physical interaction between the YgfX and FtsZ or MreB, pulldown experiments were performed using the full-length YgfX, which was fused to a His6-tag (YgfX−HIS). The cell lysate of E. coli BL21 cells expressing YgfX−HIS was mixed with the cell lysate containing FtsZ−FLAG or MreB−FLAG. Protein complexes

were purified with affinity chromatography, using Ni-NTA beads. Eluted proteins were analyzed by SDS-PAGE, and FLAG-tagged proteins were detected by Western blotting, CHIR-99021 mouse with the use of the anti-FLAG antibody (Sigma-Aldrich). As a control, a lysate containing FtsZ−FLAG or MreB−FLAG was incubated with Ni-NTA beads without YgfX−HIS. As shown in Fig. 4a, FtsZ−FLAG or MreB−FLAG was detected in the elution fractions only when it was mixed with YgfX−HIS, indicating that YgfX interacts with FtsZ and MreB. The interaction between FtsZ and YgfX was confirmed by yeast two-hybrid (Y2H) assay (James et al., 1996). The full-length and various truncated mutants of FtsZ were fused to the activation domain (AD) of pGAD-C1, while YgfX was fused to the binding domain (BD) of pGBD-C1. The interaction was assessed by monitoring the growth on selective media (SD-trp, Antidiabetic Compound Library concentration -leu, -his supplemented with 25 mM

3-aminotriazole). The growth was observed when pGBD-ygfX

was cotransformed with pGAD plasmid containing the full-length FtsZ as well as truncated variants of FtsZ, ΔC(−191), ΔC(−287), ΔN(−32), each lacking C-terminal 191, C-terminal 287, and N-terminal 31 residues, respectively (Fig. 4b). The interaction was lost when N-terminal 49 residues of FtsZ were deleted (ΔN(−49)). These results suggest that residues 33–96 of FtsZ are essential for the interaction with YgfX and that the majority click here of C-terminal residues and the first 31 N-terminal residues are dispensable for the interaction with YgfX. To directly assess the biological role of the interactions between YgfX and the cytoskeletal proteins, the effect of YgfX on in vitro polymerization of FtsZ and MreB was analyzed. To avoid the use of detergent to solubilize TM-containing full-length YgfX for polymerization assay, the soluble C-terminal 87-residue fragment (from V49 to R135) was cloned into pCold-Km. The clone was designed to express the truncated YgfX (YgfX(C)) in fusion with His6 tag at its N-terminal (YgfX(C)−HIS). YgfX(C)−HIS was produced at very high level in the cell; however, it was entirely localized in the inclusion bodies. In order to purify YgfX(C)−HIS, the insoluble fraction was collected by centrifugation and solubilized by 8 M urea. Solubilized YgfX(C)−HIS was then purified using Ni-NTA (Qiagen), which led to a high degree of purification (Fig. 5a).

, 2011). In place of the long α-helix that was found to block the MxiM pore, YscW only contains a α-helical turn. These results suggest either that the bound lipid in MxiM is an artifact of the crystallization process, which required detergents to be present, or that the lipid disruption mode of secretin insertion into membranes is not universally used by

Class 2 pilotins. Class 3 pilotins InvH, OutS, and PulS are predicted to be similar in size to the β-strand pilotins and to be predominantly α-helical, although they lack predicted TPRs (Fig. 1c). Structural data for this group are limited to the crystal structure of E. coli T2S GspS (PDB ID: 3SOL), an orthologue of the Class 3 pilotins that has not been functionally characterized. While the sequence identity among GspS, OutS, and PulS ranges from 30% to 36%, the sequence identity of InvH to OutS, PulS, and GspS is only 3%, 12%, and 14%, respectively. The structure of GspS is a http://www.selleckchem.com/products/Gefitinib.html four α-helix bundle, as is predicted for OutS and PulS (Fig. 1c). One face of GspS forms a distinct groove that could provide a convenient binding surface for an interacting partner. InvH is predicted to contain shorter α-helices and a large central region without regular secondary structure. Tertiary structure predictions by Phyre2 (Kelley selleck kinase inhibitor & Sternberg, 2009) produces high confidence models (100%) for OutS and PulS

based on GspS. As InvH is significantly different from the others at the sequence level, models can only be generated for a fragment of the protein at confidence levels of 47.3% or lower, and are not templated on GspS. Accessory DOK2 proteins that have been functionally

characterized in secretin-containing systems are listed in Table 1. Accessory proteins are not always present in a particular system, nor are their functions always the same. Many accessory proteins appear to be involved in stability of the secretin or of the secretin subunit prior to assembly. Accessory proteins that have been reported to influence secretin formation include ExeA/B in A. hydrophila; GspA/B in Vibrio species and Aeromonas salmonicida; OutB in E. chrysanthemi; MxiJ in S. flexneri; PilP in Neisseria meningitidis and P. aeruginosa; FimV in P. aeruginosa; pI/pXI in filamentous phage; BfpG in E. coli; and TcpQ in V. cholerae. In T2S, GspA/B in Vibrio species and A. salmonicida (ExeA/B in A. hydrophila) has been found to be important for expression of the secretin. However, the protein pair is not universally present – or has yet to be identified – in all T2S systems (Strozen et al., 2011). GspA spans the inner membrane and has domains in both the cytoplasm and the periplasm (Schoenhofen et al., 1998; Howard et al., 2006). A surprisingly similar arrangement and orientation is predicted for the filamentous phage accessory protein, pI, which raises the possibility that the two could be evolutionarily related.

5 mm anterior, 1.0 mm lateral from bregma, 0.5 mm deep from brain surface) of the anesthetized mouse. Initially, brief light pulses of several different light intensities (0.06, 0.3, 1.5 and 6 mW at endoscope tip) were used to determine whether any movement was evoked. If movement was detected at a certain light intensity, a light stimulation series (20 steps of light intensity) was applied. Light intensity was increased by 1.1 × at one step, and the stimuli were delivered in ascending order. At each step, light stimulation contained five 40-ms light pulses with 500-ms intervals. Whisker movements were captured at 50 frames/s with a video camera (RM-6740CL; JAI, Copenhagen,

Denmark). We classified trials as

‘single-whisker movement’, Stem Cell Compound Library where only one whisker was diffracted or a large (twice) difference was detected between the best and second-best whisker in movement amplitude at threshold. Video images were analysed using ImageJ (http://rsb.info.nih.gov/ij/) and matlab. We describe here a method for ChR2-assisted optical control of neural activity in vivo with high spatio-temporal resolution. A newly designed optical/electrical probe was used to image neurons, deliver stimulating light with high spatial resolution, and record neural activity in living animals (Fig. 2A). The device was composed of three optical fiber bundles (80 or 125 μm diameter) and 10 tungsten microelectrodes (Fig. 2B; Table 1). The probe tip had a 45 º beveled edge for minimizing brain damage. Smaller diameter electrodes (7.6 μm diameter) were gold-plated to reduce electrical impedance. The optical fiber Osimertinib ic50 bundle, which consisted Vorinostat cost of hundreds of

optical fibers, transmitted an image to a remote end (Fig. 2C). Because light propagates bidirectionally in the optical fibers, the bundle could deliver illuminating light to the neural tissue and transmit fluorescent images back to the photodetector (Fig. 2A). Each optical fiber bundle consisted of 1.9-μm-diameter single-mode optical fibers, and the spacing of each fiber was 3.3 μm, which determined the spatial resolution of a transferred image. The numerical aperture of each fiber is 0.41, and the half angle of emission from the fiber in water was approximately 10 º (Fig. 2D). A previous study showed that the spatial resolution of an optical fiber bundle-based endoscope is sufficient to visualize fluorescently labeled neurons at single-cell resolution (Vincent et al., 2006). Stimulating light was deflected by a pair of galvanometer scanners (Fig. 2A), enabling stimulating light to be sent to a single fiber core in the optical fiber bundles (Fig. 2D). This feature is important for controlling neural activity with high spatial resolution (see below). We used an in utero electroporation technique for targeted expression of ChR2 to projection neurons in layer 2/3 of the mouse cerebral cortex.

g. see Holland & Petrovich, 2005; Yin et al., 2008). This effort might be aided by multisite recordings or targeted online manipulations of key firing patterns to causally control PIT, as

well as task designs to dissociate general from outcome-specific forms of PIT (Blundell et al., 2001; Corbit & Balleine, 2005). For now, however, this work represents an important and ‘motivating’ step forwards. “
“An emerging OSI-744 purchase view of structure–function relations of synapses in central spiny neurons asserts that larger spines produce large synaptic currents and that these large spines are persistent (‘memory’) compared to small spines which are transient. Furthermore, ‘learning’ involves enlargement of small spine heads and their conversion to being large and stable. It is also assumed that the number of spines, hence the number of synapses, is reflected in the frequency

of miniature excitatory postsynaptic currents (mEPSCs). Consequently, there is an assumption that the size and number of mEPSCs are closely correlated with, respectively, the physical size of synapses and number of spines. However, several recent observations do not conform to these generalizations, necessitating a reassessment of the model: spine dimension and synaptic responses are not always correlated. It is proposed that spines are formed and shaped by ongoing network activity, www.selleckchem.com/products/pexidartinib-plx3397.html not necessarily by a ‘learning’ event, to the extent that, in the absence

of such activity, new spines are not formed and existing ones disappear or convert into thin filopodia. In the absence of spines, neurons can still maintain synapses with afferent fibers, which can now terminate on its dendritic shaft. Shaft synapses are likely to produce larger synaptic currents than spine synapses. Following loss of their spines, neurons are less able to cope with the large Masitinib (AB1010) synaptic inputs impinging on their dendritic shafts, and these inputs may lead to their eventual death. Thus, dendritic spines protect neurons from synaptic activity-induced rises in intracellular calcium concentrations. It has been postulated that dendritic spines underlie the neuronal locus of plasticity, in which long-term alterations in synaptic strength (‘memory’) are converted into persistent morphological changes. While ongoing studies attempt to characterize the nature of these morphological changes and the molecular cascades leading to them (Bhatt et al., 2009; Yoshihara et al., 2009; Holtmaat & Svoboda, 2009; Yang & Zhou, 2009; Segal, 2005), it is still not clear what constitutes a ‘memory’ at the spine level, if at all such a function can be assigned to a single dendritic spine. One major issue is whether spine morphology follows changes in ambient network activity, or does it genuinely store ‘memory’ which can be formed even after a single association between two neurons firing, irrespective of the ongoing background activity.

Infrequent diagnoses (those

with a frequency of <10 cases) were also recorded. Continuous variables were expressed as the mean and standard deviation when normally distributed, as the median and interquartile range (IQR) if distribution was skewed, and discrete variables as percentages. The Student's independent samples t-test was used to compare continuous variables and the Mann–Whitney U-test for continuous variables without a normal distribution. The association between categorical variables was evaluated using a chi-squared test (when samples were of sufficient size) or with a Fisher's exact test. Magnitude of the Everolimus supplier effect was expressed as a 95% confidence interval. A p value of <0.005 was considered statistically

significant. A total of 2,993 travelers were included in the study; 11 of them were excluded because destination did not correspond with the areas included in the study. The total number of travelers analyzed was 2,982. In total, 47.8% were women; median age was 35 years (IQR 28 to 40). Median time elapsed from return to consultation was 30 days (IQR 13 to 90). Geographical areas of travel and number of travelers to each area are shown in Figure 1. The duration of travel in order of frequency was: short term in 1,594 (53.4%), long term in 710 (23.8%), and medium term in 678 (22.7%) cases. The type of travel in order of frequency was: type A in 979 (32.8%), type B in 511 (17.1%), type C in 508 (17%), and type D in 984 (33%) C59 wnt supplier cases. The age of the traveler, duration, and type of travel depending on the geographic area visited are shown in Table 1. In total, 2,062 had received a travel-related vaccine (69.1%), and the median number of vaccines received was two (IQR: 1 to

4). In order of frequency, vaccines received were: yellow fever (79.1%), typhoid fever (55.9%), tetanus–diphtheria (44%), hepatitis B (40.6%), and hepatitis A (31.8%). Complete information was available regarding malarial chemoprophylaxis in 2,568 (86.08%) cases. In total, 1,059 (35.5%) had taken malarial chemoprophylaxis, with variations according to geographical area of travel: prophylaxis was used by 54.4% of travelers to sub-Saharan Africa, 33.5% to Central Asia Southeast, 19.4% to South America, 11.5% selleck monoclonal antibody to the Caribbean–Central America, and 5.1% to other destinations (p < 0.05). Of these 1,059, 623 (58.8%) took chemoprophylaxis correctly. This proportion varied depending on the drug used: 57 of 71 (80.3%) taking atovaquone–proguanil did so correctly, 274 of 409 (67%) taking mefloquine, 23 of 43 (53.5%) taking doxycycline, 193 of 379 (50.9%) taking chloroquine–proguanil, and 85 of 176 (48.3%) taking chloroquine; χ2 = 43.3 (p < 0.001). More than 75% of the cases had one of the following five presenting syndromes: 1,028 (34.5%) febrile syndrome, 872 (29.

, 1996). As described above, this domain contains a ‘Walker-type’ ATP-binding site (Jung & Altendorf, 1998b). Truncated forms of KdpD lacking this site (KdpD/Δ12–228, KdpD/Δ12–395) were characterized this website by a deregulated phosphatase activity. In contrast, the sole N-terminal cytoplasmic domain (KdpD/1–395)

caused constitutive expression of kdpFABC in vivo (Heermann et al., 2003a). Detailed biochemical studies revealed a stabilizing function of the N-terminal domain of KdpD in complex with phospho-KdpE and the corresponding DNA-binding site (Heermann et al., 2003a, 2009a). Many bacteria, for example the cyanobacterium Anabaena sp., have a KdpD homologue that comprises only the N-terminal domain without the C-terminal transmitter domain and the transmembrane helices (Ballal et al., 2005). Palbociclib research buy Replacement of the N-terminal domain of E. coli KdpD with the short KdpD version of Anabaena resulted in a chimera that was functional in E. coli in vivo and in vitro (Ballal et al., 2002). This result suggested that Anabaena KdpD functions in a manner similar to the N-terminal domain of E. coli KdpD. The Usp domain within the N-terminal domain functions as a binding surface for the universal stress protein UspC, and it was shown to be important for internal protein dynamics, allowing structural alterations within

KdpD upon stimulus perception (Heermann et al., 2009b). Using a ‘domain-swapping’ approach, the Usp domain within KdpD was replaced by KdpD-Usp domains of various bacteria and the six soluble universal stress proteins of E. coli, respectively. In vivo and in vitro analyses of these KdpD chimeras revealed that signaling within KdpD involves alterations of electrostatic interactions.

Chimeras containing UspF or UspG not only prevented kdpFABC expression under salt stress but also under K+ limitation, although these hybrid proteins exhibited kinase and phosphatase activities in vitro (Heermann et al., 2009a). Analysis of the predicted wild-type KdpD-Usp tertiary structure revealed that this domain has a net positively charged surface, while both UspF and UspG are characterized by net negatively charged surfaces (Heermann et al., 2009a). It is proposed that the positively CYTH4 charged Usp domain interacts with other positively charged residues in KdpD shifting the histidine kinase into the ‘ON’ state by electrostatic repulsion (Fig. 2a). Chimeras containing the negatively charged UspF or UspG remain in the ‘OFF’ state due to electrostatic attraction. A possible explanation as to why KdpD-UspF and KdpD-UspG are active in vitro, but block kdpFABC expression in vivo might be that the stabilization of the phospho-KdpE/DNA complex by the N-terminal domain of KdpD is prevented in the ‘OFF’ state (Fig. 2a) (Heermann et al., 2003a). KdpE belongs to the OmpR/PhoB response regulator family.

5b, lanes 7 and 8). The canonical three-dimensional structure of the receiver domain contains an ‘acidic pocket’ that is essential for phosphorylation of the response regulator, although only one of the aspartate residues is ultimately phosphorylated. Our results suggest that Asp58 is the conserved transphosphorylation site in AroR that, together with Asp13 and Asp53, forms the acidic pocket. Again, we used 1D 1H

NMR spectroscopy to confirm that the protein products used in these experiments were correctly folded. Arsenite-oxidizing bacteria were first identified in 1918 (Green, 1918); however, until the last decade, none were found that utilized arsenite as an energy source (Santini et al., 2000; Stolz et al., 2006). We have now demonstrated that in the chemolithoautotroph Selleck 17-AAG NT-26, the specific two-component signal transduction system is involved in the transcriptional regulation of the arsenite-oxidizing enzyme. While previously putative regulatory genes have been reported from other arsenite-oxidizing organisms, we have for the first time demonstrated the enzymatic activities of the gene products and confirmed the two proteins as a cognate response regulator pair. PS-341 The main aspect of the regulation of arsenite oxidation is that it involves σ54-dependent transcription as indicated by the presence of a σ54 promoter

region upstream of aroB and the identification of an

AAA+ protein domain, which has been linked to σ54 activation in other systems, in the response regulator AroR. Approximately Rebamipide 10% of all known DNA-binding response regulators contains the NtrC/DctD AAA+ATPase domain fused to a factor of an inversion (Fis)-type helix-turn-helix domain (Batchelor et al., 2008; Gao & Stock, 2009). ATPase in the AAA+ proteins is dependent on the formation of a hexameric or a heptameric ring structure that is regulated by phosphorylation of the receiver domain (Gao & Stock, 2009). Currently, there are two known modes of phosphorylation-induced assemblies: in the case of NtrC phosphorylated REC domain participates in the intermolecular interactions and is involved in the formation of a hexameric interface (Kostrewa et al., 1992; Sallai & Tucker, 2005; De Carlo et al., 2006), whereas in the case of NtrC1 and DctD REC phosphorylation releases the inhibitory affect that this domain has on the formation of heptameric ring and ATPase activation (Park et al., 2002; Lee et al., 2003). Further structural and mechanistic studies will be carried out addressing the molecular basis and phosphorylation dependence of AroR–DNA interaction. Arsenite sensing is particularly interesting from the aspect of bioremediation as arsenic contamination is a serious world-wide problem. In Asia (e.g. Bangladesh, several states of India, Nepal, Pakistan, Vietnam, Cambodia, China, etc.

agalactiae from DNA–DNA hybridization results. The strain possibly belonged to biovar-III; however, no strain we used was closely related to S. agalactiae by 16S rRNA gene phylogenetic analysis. We cannot speculate on the relationship between group M biovar-III and S. agalactiae, at this time. In this study, we used four strains of the group M streptococci isolated from

dogs, which belong to the biovar-II (NCTC 7760 and NCTC Navitoclax order 6400 were clearly stated as members of the biovar-II; Skadhauge & Perch, 1959). Furthermore, NCTC 7760 and NCTC 6400 were reported in the same biochemical cluster (Colman, 1968). Clearly, strains with the Lancefield group M antigen belong in different taxa. In this study, we characterize group M biovar-II streptococci and further investigations are needed to clarify the taxonomic status of the group M biovar-I and biovar-III streptococci. In summary, this biochemical and phylogenetic study demonstrated that strains PAGU 653, PAGU 1331, PAGU 1332 and PAGU 1535, corresponding to Lancefield group M biovar-II strains, represent a novel species within the genus Streptococcus. DNA–DNA hybridization confirmed that these strains were taxonomically independent species. Based on these results, these group M strains are proposed to be a novel species

of the genus Streptococcus–S. fryi sp. nov. – with Lancefield group M antigens. Streptococcus fryi (N.L. gen. masc. fryi fry’i of Fry, in honor of R.M. Fry, a bacteriologist who first AG-014699 in vitro described group M strains). Cells are Gram-positive cocci that occur in pairs or short chains. Colonies are β-hemolytic on sheep blood agar. Cells react with streptococcal group M-specific antisera. Cells are able to produce acid from glycogen, pullulan, Oxalosuccinic acid maltose and sucrose, but not from mannitol, d-sorbitol, trehalose, raffinose, d-melibiose, melezitose, l-arabinose, d-arabitol, cyclodextrin

and tagatose. Cells do not hydrolyze hippurate or aesculin, and do not produce acetoin, but hydrolyze arginine. Cells are positive for β-galactosidase, alkaline phosphatase, alanyl phenylalanyl proline arylamidase, but negative for β-glucosidase, β-glucuronidase, pyrrolidonyl arylamidase, urease, N-acetyl-β-glucosaminidase, glycyl tryptophan arylamidase and β-mannosidase. The DNA G+C content of the type strain is 38.4 mol%. The type strain PAGU 653T (=NCTC 10235T=JCM 16387T) was isolated from a dog. Table S1. Lancefield antigen group distribution in streptococcal species. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“NEIDL, Boston University, Boston, MA, USA Mycobacteriophage L5 gene 56 encodes a putative thioredoxin family protein.

agalactiae from DNA–DNA hybridization results. The strain possibly belonged to biovar-III; however, no strain we used was closely related to S. agalactiae by 16S rRNA gene phylogenetic analysis. We cannot speculate on the relationship between group M biovar-III and S. agalactiae, at this time. In this study, we used four strains of the group M streptococci isolated from

dogs, which belong to the biovar-II (NCTC 7760 and NCTC Natural Product Library ic50 6400 were clearly stated as members of the biovar-II; Skadhauge & Perch, 1959). Furthermore, NCTC 7760 and NCTC 6400 were reported in the same biochemical cluster (Colman, 1968). Clearly, strains with the Lancefield group M antigen belong in different taxa. In this study, we characterize group M biovar-II streptococci and further investigations are needed to clarify the taxonomic status of the group M biovar-I and biovar-III streptococci. In summary, this biochemical and phylogenetic study demonstrated that strains PAGU 653, PAGU 1331, PAGU 1332 and PAGU 1535, corresponding to Lancefield group M biovar-II strains, represent a novel species within the genus Streptococcus. DNA–DNA hybridization confirmed that these strains were taxonomically independent species. Based on these results, these group M strains are proposed to be a novel species

of the genus Streptococcus–S. fryi sp. nov. – with Lancefield group M antigens. Streptococcus fryi (N.L. gen. masc. fryi fry’i of Fry, in honor of R.M. Fry, a bacteriologist who first Sotrastaurin cost described group M strains). Cells are Gram-positive cocci that occur in pairs or short chains. Colonies are β-hemolytic on sheep blood agar. Cells react with streptococcal group M-specific antisera. Cells are able to produce acid from glycogen, pullulan, Meloxicam maltose and sucrose, but not from mannitol, d-sorbitol, trehalose, raffinose, d-melibiose, melezitose, l-arabinose, d-arabitol, cyclodextrin

and tagatose. Cells do not hydrolyze hippurate or aesculin, and do not produce acetoin, but hydrolyze arginine. Cells are positive for β-galactosidase, alkaline phosphatase, alanyl phenylalanyl proline arylamidase, but negative for β-glucosidase, β-glucuronidase, pyrrolidonyl arylamidase, urease, N-acetyl-β-glucosaminidase, glycyl tryptophan arylamidase and β-mannosidase. The DNA G+C content of the type strain is 38.4 mol%. The type strain PAGU 653T (=NCTC 10235T=JCM 16387T) was isolated from a dog. Table S1. Lancefield antigen group distribution in streptococcal species. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“NEIDL, Boston University, Boston, MA, USA Mycobacteriophage L5 gene 56 encodes a putative thioredoxin family protein.

, 2002; Kang et al., 2007). These products with high biological activity can severely attack cell membranes, proteins and nucleic acids, cause enzyme inactivation, protein denaturation, lipid peroxidation and DNA mutation, and result in ecotoxicity through oxidative damage to cellular components (Imlay et al., 1998; Vandana et al., 2002). Therefore, mechanisms that protect the cell against the toxic effects of ROS such

as H2O2 and are needed. Many cells have developed an antioxidative defense system consisting of ROS-scavenging enzymes, e.g. SOD, CAT, ascorbate peroxidase (APX), and antioxidants such as ascorbate (AsA) and glutathione (GSH) (Mittler et al., 2004). Various antioxidant enzymes, whose function is to eliminate Selleck Dinaciclib oxygen free radicals and protect the organism, indirectly could reflect the changes of oxygen free radical content in living cells. SOD can catalyze to O2 and H2O2 rapidly (Gerlach et al., 1998) and then H2O2 is eliminated by the H2O2-scavenging enzyme CAT (Hidalgo et al., 2004). Among cellular functions, GST plays an important role in the detoxification of ROS and the regulation of redox balance (Siritantikorn et al., 2007). Total antioxidant capacity (T-AOC), which

is defined as a measure of the amount of free radical scavenging (MacDonald-Wicks et al., 2006), is a useful parameter to assess the antioxidant status of an organism. Microorganisms

frequently undergo stress conditions caused by herbicide Obeticholic Acid application (Lü et al., 2009). Bacteria possess a wide variety of stress responses, including oxidative stress response, and they have the ability to sense the stress signal through a process in which many enzymes are involved (Niazi et al., 2008). There is considerable interest in free radical-mediated damage in biological systems following atrazine exposure. However, these studies focused mainly on damage to animals and plants cells. Few studies have shown the response of antioxidant enzymes in bacteria to the oxidative stress induced by atrazine. Moreover, information on general stress responses Clomifene and their regulation in bacteria is limited. The purpose of the present work is to evaluate the response of antioxidant enzymes in two representative bacteria to atrazine stress. SOD, CAT, GST activities and T-AOC in one Gram-negative representative strain Escherichia coli K12 and one Gram-positive representative strain Bacillus subtilis B19 treated with atrazine were examined in this study. We believe that this work will be valuable for further study on atrazine stress tolerance of bacteria and defense mechanism of antioxidant enzymes against atrazine or other triazine herbicides.