Figure 1 shows a diagram illustrating the malX-malI intergenic region with the transcription GSK3235025 datasheet start sites for the malX and malI promoters, the corresponding −10 elements, and the DNA site for CRP that is located at position −41.5 with respect to the malX transcription start and position −43.5 with respect to the malI transcription start. Figure 1 also shows the locations of two 16 base pair elements, suggested to be the operator targets for the MalI repressor. The aim of the work described here was to investigate this suggestion and to determine the functional operator(s) for each promoter. In a previous

work, Lloyd et al. (2008) described how the malX promoter could be assayed by cloning the malX100 fragment into the lac expression vector plasmid, pRW50. Measurements of β-galactosidase expression in M182 or its Δcrp derivative showed the malX promoter to be a typical Class II CRP-dependent promoter, which is consistent with the location of the DNA site for CRP (West et al., 1993). Lloyd et al. (2008) also reported that expression of the malX promoter∷lac fusion carried by pRW50 is unaffected by the introduction of a multicopy plasmid carrying the malX-malI intergenic region, suggesting that the level of chromosomally

encoded MalI is insufficient to repress the malX promoter significantly. Thus, to set up a system to measure MalI-dependent repression of the malX promoter, we cloned the malI gene into plasmid pACYC184 to generate pACYC-malI. Reverse transcriptase Measurements of β-galactosidase expression in M182 cells carrying buy Stem Cell Compound Library pRW50 with the malX100 promoter show that the presence of pACYC-malI causes an ∼30-fold reduction in expression, compared with the control with the empty pACYC-ΔHN plasmid (Table 1, upper panel). The experiment was then repeated with M182 cells carrying pRW50 with the malX400 promoter fragment, in which the malX promoter sequence upstream of the DNA site for CRP had been removed (illustrated in Fig. 1). The data in Table 1 (upper panel) show that neither malX promoter

activity nor repression by MalI is substantially affected by the deletion, and thus sequences upstream of the DNA site for CRP must play little or no role. On MacConkey lactose indicator plates, colonies of M182 carrying pRW50 with either the malX100 or malX400 promoter fragments, together with pACYC-malI, appear as white Lac− colonies. In contrast, if pACYC-malI is replaced with pACYC-ΔHN, colonies have a bright red, clear Lac+ appearance. Thus, to pinpoint the operator sequences essential for repression of the malX promoter by MalI, we used error-prone PCR to generate a library of random mutations in the malX400 promoter fragment and screened for mutations that resulted in pink or red colonies of cells containing pACYC-malI. We reasoned that such colonies would contain pRW50 carrying the malX400 fragment with mutations that interfered with MalI binding.

This hypothesis is also supported by the fact that unimanual force regulation with the contralateral thumb was unable to induce the observed modulation of TCI. The most plausible explanation for our results may be the characteristics of the present task in which bilateral homonymous muscles (i.e. APBs) acted as the prime movers in the symmetric and asymmetric conditions. Even while a muscle force is gradually released, the M1 is likely to play an important role in the regulation of an isometric force (Toma et al.,

1999; Spraker et al., 2009). Therefore, it might not be an appropriate strategy for the isometric force regulation task to simply suppress the activity of the contralateral M1. As another possibility, visual information might be C59 wnt solubility dmso involved in our findings. Visual feedback from an action has been demonstrated to have a prominent effect on the stability of bimanual coordination (Byblow et al., 1999; Mechsner et al., 2001). In the present study, the required movement of the force line was identical between the symmetric and asymmetric conditions to perform force regulation with as equal accuracy as possible (‘Materials and methods’). Accordingly, the mapping rule for transforming the direction of force to the direction of the line movement on the oscilloscope was quite different across the symmetric and asymmetric conditions. The congruency of the visual feedback and the actual behavior

has a severe JAK phosphorylation impact on the excitability of cortical motor circuits (Johansson et al., 2006). Furthermore, the interhemispheric neural interactions seem to be influenced by the action direction in the extrinsic coordinated frame. The magnitude of interhemispheric interactions changes according to whether the direction of a side of action is egocentrically congruent to that of the contralateral tested side (Duque et al., 2005; Yedimenko & Perez, 2010). Therefore, if the external framework of a hand action is involved in the neural processing of visual information, the mechanism of visuomotor transformation might influence the

excitability of the transcallosal circuits. Using static contraction of bilateral index finger muscles, Yedimenko & Perez (2010) recently demonstrated that interhemispheric inhibition was larger when both the left and right index Fossariinae finger forces are directed toward the body midline compared with when left and right forces are directed in the same direction with respect to an allocentric coordinated frame. This result is in agreement with our findings that interhemispheric inhibitory interactions changed according to the direction of the left and right forces. However, care should be taken to interpret the symmetry of the force directions. According to the allocentric coordinated frame (i.e. parallel movements are recognized as symmetrical), the previous finding is compatible with ours (Yedimenko & Perez, 2010).

The deprivation started immediately after stroke and lasted 7 days. This procedure, in control (non-stroke) animals, results in an enlargement of functional representation of the spared row, as shown with [14C]2-deoxyglucose uptake mapping. In mice with stroke induced by photothrombosis in the vicinity of the barrel cortex,

vibrissae deprivation did not result in an enlargement of the cortical representation of the spared row C of vibrissae, which confirmed our previous results. However, when mice were injected with the broad-spectrum inhibitor of MMPs FN-439 (10 mg/kg, i.v.) immediately before a stroke, an enlargement of the representation of the spared row similar to the enlargement found in sham mice was observed. These results indicate the involvement Z-VAD-FMK mw of MMPs in the impairment of use-dependent plasticity in the vicinity of an ischaemic lesion. “
“Estradiol and progesterone interact with the dopaminergic and other neurotransmitter systems that are involved

in the processing of rewards. On the systems level, these hormones modulate responses to stimulants as well as neuronal activity related to the anticipation of monetary gains. As different mechanisms might underlie the processing of gains and losses, the current study aims to investigate whether neural correlates of gain and loss anticipation are differentially 5-Fluoracil cost modulated by menstrual cycle phases. Therefore, young, naturally cycling women were examined by means of functional neuroimaging during performing a modified version of the ‘Monetary Incentive Delay’ task in the early follicular and in the luteal menstrual cycle phase. During the low hormone early follicular phase, the anticipation of high vs. low gains

and losses was associated with activity in a largely overlapping network of brain areas. However, high hormone levels in the luteal phase affected brain activity in these areas differentially during the anticipation of high vs. low gains and losses. In particular, the orbitofrontal cortex showed a reduced sensitivity to gain magnitude, whereas the ventral striatum and the anterior cingulate showed a reduced sensitivity to loss magnitude. In summary, the high amount of progesterone and estradiol in the luteal phase decreased activity O-methylated flavonoid related to the anticipation of monetary gains and losses in different brain areas, suggesting that hormones modulate different processes during the anticipation of gain and loss magnitude. “
“During brain development, many factors influence the assembly and final positioning of cortical neurons, and this process is essential for proper circuit formation and normal brain function. Among many important extrinsic factors that guide the maturation of embryonic cortical neurons, the secreted neurotransmitter GABA has been proposed to influence both their migratory behaviour and their terminal differentiation.

Furthermore, mitochondrial OXPHOS and oxidative stress measurements in PBMCs may not necessarily reflect mitochondrial dysfunction in the dorsal root ganglion or sural nerves. Nevertheless, some important conclusions are possible. The correlation of ENFD to previously established

risk factors for neuropathy, namely age and height, lends credibility to ENFD as a valid predictive marker of neuropathy risk. Lower CD4 cell counts BTK inhibitor screening library and higher OXPHOS CIV activity levels are found in association with subclinical peripheral nerve damage in HIV-infected ARV-naïve individuals with moderate to severe HIV immunodeficiency. Whether HAART regimens with less mitochondrial toxicity can repair such damage has yet to be determined. Furthermore, pre-existing

subclinical ENFD damage may have clinical consequences if it lowers the threshold for the development of clinical neuropathy upon exposure to d4T or other neurotoxic medications Rucaparib and conditions. The authors wish to thank the patients for their participation in this study. Additionally, we would like to acknowledge the specific contributions to the study by Stephen J. Kerr, Patcharawee Rungrojrat, Somsong Teeratakulpisarn, and Tippawan Pankam from SEARCH/TRCARC and Daniel E. LiButti, Julia Choi and Heidi Fink from the University of Hawaii. The biostatistician for the study was Victor DeGruttola, Harvard School of Public Health, Boston, MA, USA. Funding was received from the Thai Government Pharmaceutical Organization, the National Institute of Health [R01NS063932 (CMS), R01AI074554 (MG),

and P20RR011091 U54RR026136], Gilead Sciences, and MitoScience Inc. [P30MH075673 (JCM) and NS44807 (JCM)]. “
“Antiretroviral (ARV) therapy has prolonged the life expectancy of HIV-infected persons, increasing their risk of age-associated diseases, including atherosclerosis (AS). Decreased risk of AS has been associated with the prevention and control of hypertension (HTN). We conducted a cohort study of perimenopausal women and older men with or at risk of HIV infection to identify risk factors CYTH4 for incident HTN. Standardized interviews, physical examinations, and laboratory examinations were scheduled at 6-month intervals. Interview data included demographics, medical, family, sexual behaviour and drug use histories, and physical activity. There were 330 women and 329 men eligible for inclusion in the study; 27% and 35% of participants developed HTN during a median follow-up period of 1080 and 1071 days, respectively. In gender-stratified analysis, adjusting for traditional HTN risk factors (age, race, body mass index, smoking, diabetes, family history of HTN, alcohol dependence, physical activity and high cholesterol), HIV infection was not associated with incident HTN in women [hazard ratio (HR) 1.31; 95% confidence interval (CI) 0.56, 3.06] or men (HR 1.67; 95% CI 0.75, 3.74).

lactis ssp. cremoris SMBI198, a strain derived from NZ9000, knocked out in the chromosomal htrA gene (Poquet et al., 2000; Rigoulay et al., 2004). The resulting strain produced only a surface-associated Inhibitor Library cost form of the recombinant flagellin (Fig. 1b). Interestingly, two bands showed homology with B. cereus flagellin, one of around 45 and the other one of around 63 kDa. It is known that, in certain cases, protein aggregates are difficult to disassociate, producing this kind of artefact

in SDS-PAGE (Kankainen et al., 2009). This tendency to aggregation may lead to bacterial autoaggregation, and the physical–chemical dynamics of this process are currently under investigation. This could reflect the trend to auto-assembly that flagellins display in vivo (Hueck, 1998). In addition, it reinforces the role of HtrA as the major housekeeping protease on the L. lactis surface as, in the absence of it, the aggregated flagellin cannot be proteolyzed and thus shed into the bacterial surroundings. Lactococcuslactis ssp. cremoris CH showed a better ability to adhere to mucin when flagellin production was induced with nisin (Fig. 2). Adhesion of both

L. lactis ssp. cremoris SMBI198 and L. lactis ssp. cremoris SMBI198 (pNZ8110) strains was similar to uninduced L. lactis ssp. cremoris CH cultures (data not shown). After gene induction, the adhesion was increased by a factor selleck of 4.7. Nisin-induced L. lactis CH cultures inhibited the adhesion to mucin of the two enteropathogens used in this study in a dose-dependent manner (Fig. 2). A lower inhibition was also observed when uninduced L. lactis ssp. cremoris

CH cultures were used. This is not surprising as L. lactis is also able to bind to mucin; an interference with enteropathogen adhesion to mucin is thus expected. The adhesion data, corrected by the inhibitory effect observed for the uninduced L. lactis CH strain cultures, showed that L. lactis ssp. cremoris CH expressing the Bacillus flagellin was able to inhibit the adhesion of E. coli 4.4 times (1.8 times in the case of uninduced cultures), and 3.9 times in the case of S. enterica (1.6 times in the case of uninduced cultures), when the E. coli/L. lactis ratio was 1 : 10. In our previous work, we showed that adhesion of B. cereus CH to mucin could be explained, Ibrutinib in vitro to a large extent, by the presence of a flagellin on its surface (Sánchez et al., 2009a). Flagella have been proposed as important factors for bacterial adhesion to mucosal surfaces (Rumbo et al., 2006), and are glycosylated in several microorganisms (Ewing et al., 2009; Hayakawa et al., 2009; Konishi et al., 2009; Logan et al., 2009). One B. cereus strain lacking the flhA gene, which results in the absence of flagella, presented a lower adhesion to both Caco-2 and HeLa cell lines (Ramarao & Lereclus, 2006). In addition, monomeric flagellins detached from the cell surface have been proposed as the soluble probiotic factor secreted by the strain E. coli Nissle 1917.

pseudomallei invasion into A549 epithelial cells, suggesting that it is an important virulence

factor of the pathogen. Selleckchem Veliparib BopC is conserved in B. pseudomallei and B. mallei, but absent from the related avirulent B. thailandensis. Thus, it is tempting to speculate that the acquisition of BopC was an important step in the evolution of the pathogenic Burkholderia spp. We gratefully acknowledge a financial support from the National Science and Technology Development Agency (Grant No. BT-B-01-MG-14-5123 to S.K.) and the Royal Golden Jubilee Ph.D. Program (Grant No. PHD0151/2549 to S.M. and S.K.). G.N.S is supported by a grant from MRC. N.L.A. is supported by a grant from the Wellcome Trust. Tanapol Wangteeraprasert is acknowledged for his support on construction of pTrc1517His. S.M. and S.K. contributed equally to this work. “
“One of the issues facing the nuclear power industry is how to store spent nuclear fuel which

is contaminated with radionuclides produced during nuclear fission, including caesium (134Cs+, 135Cs+ and 137Cs+) and cobalt (60Co2+). In this study, we have isolated Co2+- and Cs+-resistant bacteria from water collected from a nuclear fuel storage pond. The most resistant Cs+ and Co2+ isolates grew in the presence of 500 mM CsCl and 3 mM CoCl2. Strain Cs67-2 is resistant to fourfold more Cs+ than Cupriavidus Bortezomib solubility dmso metallidurans str. CH34 making it the most Cs+-resistant strain identified to date. The Cs+-resistant isolates were closely related to bacteria in the Serratia and Yersinia genera, while the Co2+-resistant isolates were closely related to the Curvibacter and Tardiphaga genera. These new isolates could be used for bioremediation. “
“Long-term spaceflights will eventually become an inevitable occurrence. Previous studies have indicated that oral infectious diseases, including dental caries, were more prevalent in astronauts due to the

effect of microgravity. However, the impact of the space environment, especially the microgravity environment, on the virulence factors of Streptococcus mutans, a major caries-associated bacterium, is yet to be explored. In the present BCKDHA study, we investigated the impact of simulated microgravity on the physiology and biofilm structure of S. mutans. We also explored the dual-species interaction between S. mutans and Streptococcus sanguinis under a simulated microgravity condition. Results indicated that the simulated microgravity condition can enhance the acid tolerance ability, modify the biofilm architecture and extracellular polysaccharide distribution of S. mutans, and increase the proportion of S. mutans within a dual-species biofilm, probably through the regulation of various gene expressions. We hypothesize that the enhanced competitiveness of S. mutans under simulated microgravity may cause a multispecies micro-ecological imbalance, which would result in the initiation of dental caries.

NNH was calculated as the reciprocal of the difference between the underlying risks of MI with and without abacavir use. A parametric statistical model was used to calculate the underlying risk of MI over 5 years. The relationship between NNH and Bleomycin in vivo underlying risk of MI is reciprocal, resulting in wide variation in the NNH with small changes in underlying risk of MI. The smallest changes in NNH are in the medium- and high-risk groups of MI. The NNH changes as risk components are modified;

for example, for a patient who smokes and has a systolic blood pressure (sBP) of 160 mmHg and a 5-year risk of MI of 1.3% the NNH is 85, but the NNH increases to 277 if the patient is a nonsmoker and to 370 if sBP is within the normal range (120 mmHg). We have illustrated that the impact of abacavir use on risk of MI varies according to the underlying risk and it may be possible to

increase considerably the NNH by decreasing the underlying risk of MI using standard of care interventions, such as smoking cessation or control of hypertension. Abacavir is a common antiretroviral used in the treatment of HIV-1 infection and is currently recommended as one of the possible components of initial combination antiretroviral treatment [1–3]. The D:A:D study group recently reported an increased risk of myocardial infarction (MI) related to current or recent use of abacavir [4,5]. Some of the HIV-1 treatment guidelines have already taken into account the click here clinical implications of the D:A:D findings by emphasizing that clinicians should consider PI-1840 careful assessment of patients who are on abacavir and at high risk of MI [2,6,7]. It is therefore of great importance

to ensure that the risk of MI attributed to abacavir use, together with the underlying risk of MI, is correctly interpreted and understood. Presenting results as relative risks (RRs) is standard in observational studies [8], but may be difficult to translate into clinical practice. The number needed to treat (NNT) and absolute risk reduction may be more clinically relevant, when assessing the beneficial effect of treatment [9–11], and the number needed to harm (NNH), together with absolute risk increase (ARI), will better reflect any adverse effect of treatment than RR in clinical terms [12]. Both NNH and RR are measures that attempt to summarize two numbers (the risks of MI with and without abacavir). RR summarizes the relative increase in the underlying risk of an event according to whether the patient receives a given treatment or not and the NNH indicates the number of patients that need to be treated to observe the adverse effect of a treatment in one additional patient. This approach was first proposed in 1988 [13], but it is still infrequently used to describe risk of adverse events of medicines [14–17]. NNH is a tool that can be used in different settings [18].

repeated deviant), repetition probability (high vs. low) and temporal regularity (anisochronous vs. isochronous). To check for differences in the distribution of MMN as a function of repetition and/or repetition probability, four regions of interest (ROIs) were defined: left (F5,

FC5, C5); center-left (F1, FC1, C1); center-right (F2, FC2, C2); and right (F6, FC6, C6). Scalp potential (SP) measures and scalp current density (SCD) values were computed for each ROI as the mean across electrode locations. Voltage measures were transformed into current density estimates by computing the second spatial derivative of the interpolated voltage distribution (Perrin et al., 1989, 1990), with maximum degree of Legendre polynomials Selleck GDC0199 set to 50, order of splines (m) equal to 4, and a smoothing parameter of 10−5. This way we obtained reference-free distribution maps of local current sources/sinks (radial current flow through the skull measured in mA/m3; R428 Srinivasan, 2005). Four-way anovas with factors repetition, repetition probability, laterality (central vs. lateral) and side (left vs. right) were separately run for each temporal regularity condition on SP measures and SCD estimates. IBM SPSS Statistics for Windows, Version 20.0 (IBM; Armonk, NY, USA) was used for statistical analyses. Brain electrical tomographic procedures

were applied to detect the presence of differences in MMN generator location, using the distributed inverse solution VARETA approach (Variable Resolution Electrical Tomography; Bosch-Bayard et al., 2001). VARETA reconstructs brain sources by estimating the spatially smoothest intracranial primary current density (PCD) distribution that is compatible with the observed scalp voltages, and restricts the allowable solutions to the gray matter on the basis of probabilistic Montréal Neurological either Institute (MNI) 3D brain tissue maps (Evans et al., 1993; Trujillo-Barreto et al., 2004). Statistical parametric maps (SPMs) of the PCD estimates were then constructed based

on a voxel by voxel Hotelling T2 test against zero (threshold: P < 10−4) to determine the sources of the MMN component separately for each condition and for the relevant contrast between solutions. The PCD is a vector quantity, that is, at each voxel the three projections of the PCD vector onto the three orthogonal directions in the 3D Cartesian space are estimated. This asks for a multivariate T2 statistic at each voxel to test for changes in magnitude as well as orientation of the PCD vector. Significance threshold correction to account for spatial dependencies between voxels was calculated by means of random field theory (Worsley et al., 1996). Results are shown as 3D images. To verify if indeed a slower stimulus rate (SOA = 600 ms, 1.

Cells were grown in the standard Sauton medium or liquid NB (nutrient broth) medium, as well as in the modified Hartman-de-Bont medium (Shleeva et al., 2004) or modified SR-1 medium (Anuchin et al., 2009) as described below. In standard CFU assays, aliquots of decimally diluted cell suspensions were plated on solid NB medium. The Δhlp strain and recombinant strains (Table 1) were maintained on the NB medium with 10 μg mL−1 kanamycin and grown under the same conditions as the Wt strain. The hlp gene was amplified by PCR using the forward primer 5′-GTGGATCCTGGAAATCAGTGGTCACAG-3′

and the reverse primer 5′-ATCTGCAGCCTCCCGACGAGAAGTAACG-3′ (BamHI and PstI restriction GSK3 inhibitor sites are in bold). The purified PCR product was ligated into the pGEM-T vector (Promega), resulting in pGEM-hlp, which was introduced into E. coli strain DH5α. Transformed clones were selected and examined by PCR. Thereafter, pGEM-hlp and pMind were digested with restriction enzymes BamHI and

PstI and the hlp fragment was ligated into the pMind vector. The ligated product pMind-hlp was introduced into E. coli strain DH5α, and the sequence of the cloned gene was confirmed. All vectors were introduced into E. coli by electroporation according to the BioRad this website protocol; to incorporate the vectors in M. smegmatis cells, we used the procedure as described elsewhere (Parish & Stoker, 1998). A truncated form of Micrococcus luteus Rpf, named RpfSm, served as an additive in resuscitation medium. RpfSm contained the conserved Rpf domain followed by 20-aa fragment of variable domain: ATVDTWDRLAECESNGTWDINTGNGFYGGVQFTLSSWQAVGGEGYPHQASKAEQIKRAEILQDLQGWGAWPLCSQKLGLTQADADAGDVDATE. The truncated gene was amplified by PCR from the pET-19b-Rpf (Mukamolova et

al., 1998), using the T7 promoter primer: GCGAAATTAATACGACTCACTAT and the reverse primer: CGACGGATCCTCACTCGGTGGCGTCACGT (the BamH1 restriction site is marked in bold). The purified PCR product was digested with XbaI and BamH1, purified and ligated into pET19b vector, which was introduced in E. coli DH5α. The construct, containing the truncated rpf gene (rpfSm), was sequenced and used to transform E. coli HSM174 (DE3). RpfSm was purified from 350 mL cultures of E. coli producer strain grown at 37 °C in the rich medium Cyclin-dependent kinase 3 (HiMedia) with ampicillin (100 μg mL−1) to OD600 nm 0.65–0.8. After induction with 1 mM IPTG, growth was continued for 2 h at room temperature. Cells were harvested by centrifugation at 3000 g for 15 min and frozen in binding buffer (BB) (20 mM Tris-HCl, pH 8.0; 0.5 M NaCl; 5 mM imidazole). Thawed cell suspensions in 10 mM MgSO4 were treated with RNAse and DNAse at concentrations 10 μg mL−1 each and then with 8 M urea. After sonication, the crude extract was centrifuged at 6000 g for 30 min to remove cell debris, and supernatant was applied onto a 2-mL Ni2+-chelation column (Sigma) equilibrated with BB.

coli colonies with CR (Hammar et al., 1995). CR staining of E. coli colonies was not observed for the mlrA mutant (data not shown), supporting the prediction that curli fimbriae were not produced in the mlrA mutant. Three positive factors, IHF, OmpR and RstA, can associate simultaneously within the promoter-proximal click here hot-spot II region of transcription factor binding (Fig. 6), and cooperate with each other for activation of the csgD promoter. On the other hand, two negative factors, CpxR and H-NS, also

bind to the same region and collaborate with each other (Ogasawara et al., 2010). As the enhancement of csgD mRNA synthesis by overproduction of MlrA was not observed in the ompR and ihf mutants, we then examined the possible interplay between MlrA, OmpR and IHF. The results indicated that MlrA binds in the spacer region between promoter-distal transcription factor-binding hot-spot I (including IHF-site I) and promoter-proximal hot-spot Y 27632 II (including IHF-site 2), to which OmpR also binds (Fig. 6). Gel shift assays using the CD6 probe DNA indicated that each of MlrA, OmpR and IHF alone formed CD6 complexes (Fig. 5a and b, lanes 2–11). In

pair-wise assays, MlrA was found to bind together with either OmpR or IHF (Fig. 5a and b, lanes 12–16). In the simultaneous presence of MlrA, OmpR and IHF, all three regulators bind to the same CD6 probe forming MlrA–OmpR–IHF–DNA quaternary complexes (Fig. 5c). Together, we concluded that the three positive regulators, MlrA, IHF and OmpR, function independently, and do not show strong cooperation. Plasmid-encoded ADP ribosylation factor regulatory protein MerR was isolated as a mercury ion resistance gene (Ni’ Bhriain et

al., 1983; Lund et al., 1986; Heltzel et al., 1987). The MerR family of prokaryotic transcriptional activators have been identified in various bacteria except for E. coli and have a common molecular design, but have evolved to recognize and respond to different metals (Barkay et al., 2003; Brown et al., 2003; Hobman, 2007). MerR controls transcription of a set of genes (the mer operon) conferring mercury resistance. Homodimeric MerR represses transcription in the absence of mercury and activates transcription upon Hg(II) binding (Guo et al., 2010). One unique property of MerR is its ability to underwind DNA, resulting in activation of the target promoters by modulating the distance between promoter −35 and −10 (O’Halloran et al., 1989; Ansari et al., 1992). In addition, MerR was suggested to make interact directly with RNA polymerase (Kulkarni & Summers, 1999; Brown et al., 2003) as in the case of other class-I and class-II transcription factors (Igarashi & Ishihama, 1991; Ishihama, 1992, 1993; Busby & Ebright, 1999). MlrA contains a conserved N-terminal DNA-binding domain present in members of the MerR family, implying the mode of MlrA action should be the same with that of other MerR family transcription factors.