Patients should also be informed about the possibility of virological failure leading to transmission of HIV. Decisions on condom use and safer sex should always be based on a recent VL test result and not on an assumption that taking ART implies non-infectiousness. For serodiscordant heterosexual couples wishing to conceive, irrespective of the method used for conception, the HIV-positive partner will need to be on ART with an undetectable plasma VL, regardless of

his/her CD4 cell count BGB324 supplier or clinical status. This is likely to reduce the risk of transmission sufficiently to be the only risk-reduction method some couples will want, but additional measures such as sperm washing, artificial insemination and potentially pre-exposure prophylaxis (PrEP) to the HIV-negative partner have either been recommended in previous guidance [55] or are currently being assessed for couples wishing to address concerns of any residual risk of transmission. Details of the use of ART to prevent mother-to-child transmission are covered in the BHIVA guidelines for the management of HIV infection in pregnant women 2012 [56]. “
“1. Levels of evidence 1.1 Reference 2. Introduction 3. Auditable targets 4. Table EPZ-6438 order summaries 4.1 Initial diagnosis

4.2 Assessment of ART-naïve individuals 4.3 ART initiation 4.4 Initial assessment following commencement of ART 4.5 Routine monitoring on ART 4.6 References 5. Newly diagnosed and transferring HIV-positive individuals 5.1 Initial HIV-1 diagnosis 5.2 Tests to determine whether acquisition of HIV infection is recent 5.3 Individuals transferring care from a different HIV healthcare setting 5.4 Communication with general practitioners and shared care 5.5 Recommendations 5.6 References Tryptophan synthase 6. Patient history 6.1 Initial HIV-1 diagnosis 6.2 Monitoring of ART-naïve patients 6.3 Pre-ART initiation assessment 6.4 Monitoring individuals established on ART 6.5 Assessment of adherence 6.6 Recommendations 6.7 References 7. Examination 7.1 Recommendations 8. Identifying

the need for psychological support 8.1 References 9. Assessment of immune status 9.1 CD4 T cell counts 9.2 CD4 T cell percentage 9.3 References 10. HIV viral load 10.1 Initial diagnosis/ART naïve 10.2 Post ART initiation 10.3 Individuals established on ART 10.4 Recommendations 10.5 References 11. Technical aspects of viral load testing 11.1 References 12. Viral load kinetics during ART and viral load ‘blips’ 12.1 References 13. Proviral DNA load 13.1 References 14. Resistance testing 14.1 Initial HIV-1 diagnosis 14.2 ART-naïve 14.3 Post treatment initiation 14.4 ART-experienced 14.5 References 15. Subtype determination 15.1 Disease progression 15.2 Transmission 15.3 Performance of molecular diagnostic assays 15.4 Response to therapy 15.5 Development of drug resistance 15.6 References 16.

001); however, this increase was only able to restore the biofilm defect of the ΔnspS strain to levels of the wild-type cells that did not overexpress nspC (Fig. 4a). Planktonic cell density was not affected. To determine whether vps gene transcription was also affected by increased NspC levels, we measured the activity of the vpsL promoter making use of a vpsL-lacZ chromosomal fusion in this strain. Increased NspC levels led to 4.7- and 2.5-fold higher β-galactosidase activity in log- and stationary-phase cells, respectively (Fig. 4b). To determine whether the increases in biofilm cell density and vps gene transcription

could be explained by an effect on the intra- or extracellular polyamine pools, we quantified www.selleckchem.com/products/gsk2126458.html the polyamines in these strains and the spent medium and found that increased levels of NspC did not lead to any alterations in polyamine levels (Fig. 4c and d). These results indicate

that NspS is not required for the stimulatory effect of increased NspC levels on biofilms and vps gene expression. In this work, we have demonstrated that increased levels of the enzyme NspC lead to a significant increase in biofilm formation in a vps-dependent manner in V. cholerae O139. In addition, increased NspC levels result in a decrease in motility, indicating that NspC levels have opposing effects on biofilms and motility. Norspermidine concentrations in click here the cells do not change in response to increased NspC levels. This finding corroborates previous studies on polyamine metabolism in other organisms; for example, overexpression of S-adenosylmethionine decarboxylase, which is involved in spermidine biosynthesis in plants, does not lead to changes in polyamine levels in the cell (Hanfrey et al.,

2002). In both prokaryotes and eukaryotes, polyamine homeostasis is maintained by a variety of regulatory mechanisms including import, export, degradation, and interconversion Baricitinib of polyamines, feedback inhibition of polyamine synthesis enzymes by end products, and transcriptional regulation of genes encoding proteins involved in polyamine metabolism and transport (Persson, 2009; Igarashi & Kashiwagi, 2010). In Vibrio alginolyticus, norspermidine was shown to inhibit all three enzymes involved in the synthesis of norspermidine (Nakao et al., 1991). The V. cholerae and V. alginolyticus enzymes share approximately 82% amino acid sequence identity; therefore, it is likely that the V. cholerae enzymes are also regulated by feedback inhibition by norspermidine. Therefore, product feedback inhibition could contribute to maintaining norspermidine levels and partially account for the lack of an increase in cellular norspermidine levels in the nspC overexpression strain. It is also highly likely that limitations in the levels of the NspC substrate carboxynorspermidine could also prevent increased production of norspermidine.

It has previously been shown that orsA (AN7909) is involved in the formation of orsellinic acid (2), lecanoric acid (15), the two colored compounds F-9775A (16) and F-9775B (17), orcinol, diorcinol, gerfeldin and deoxy-gerfeldin. (Schroeckh et al., 2009; Sanchez et al., 2010). Our analysis confirms the link between orsellinic acid, lecanoric acid, diorcinol, F-9775A, F-9775B to orsA as these compounds are missing in the orsAΔ strain. However, we have not been able to detect the gerfeldins in any of our strains, and apparently our conditions favor violaceol and not gerfeldin

formation. The violaceols are formed by dimerization of two C7 monomers of 5-methylbenzene-1,2,3-triol, a compound that we could tentatively detect as [M-H]− at m/z 139 in cultivation find more extracts. The C7 backbone of 5-methylbenzene-1,2,3-triol, check details may conceivably be formed by decarboxylation of a C8 aldol intermediate as suggested by Turner 40 years ago (Turner, 1971) (Fig. 5). This C8 intermediate also serves as a branch point towards orsellinic acid. Interestingly, the same compounds that disappear in the orsAΔ strain also disappear in AN7903Δ, a strain missing a PKS gene separated from orsA by only ∼20 kb (Fig. 4). This result does not contradict the original assignment of orsA as the PKS gene responsible for production of orsellinic acid. Although the enzymes encoded by the two genes are predicted

to share many of the same functional domains, AN7903 is larger by around 500 amino acid residues and contains a methyl-transferase domain, which is not required for orsellinic acid production. Moreover, we note that Schroeckh et al. (2009) observed that both AN7903 and orsA were upregulated when orsellinic acid was induced by co-cultivation with Streptomyces hygroscopicus,

indicating cross-talk between the two clusters. Surprisingly, what appear to be trace amounts of orsellinic acid can be detected as m/z 167 [M-H]− in both the AN7903Δ and the orsAΔ strains (Fig. 4). The source of this residual orsellinic acid remains elusive, but it could possibly stem RG7420 from unmethylated byproducts from the PKS, AN8383, that produces 3,5-dimethylorsellinic acid, see below. Interestingly, production of austinol (18) and dehydroaustinol (19) was observed in the reference strain on several media (Fig. 1). Despite the fact that the production of these compounds is known from A. nidulans (Szewczyk et al., 2008), they have not yet been assigned to a specific gene. Only the AN8383Δ strain failed to produce the two austinols on all the media, which triggered austinol production in the reference strain (Fig. 6a). This, phenotype could be rescued by inserting the structural gene of AN8383 under the control of the gdpA promoter into an ectopic locus, IS1 (Hansen et al., 2011) (Fig. 6a). Moreover, a point mutant strain AN8383-S1660A also failed to produce austinols on these six media (Fig. 6a).

Most patients, 90% of them, have no family Forskolin mw history and are considered to have the sporadic form of ALS. Currently, there is no cure for ALS. One drug, riluzole, has been demonstrated to significantly increase survival and is well tolerated, but the magnitude of its effect is limited (Bensimon et al., 1994; Lacomblez et al., 1996; Tripathi & Al-Chalabi, 2008). Symptomatic therapy remains the mainstay of treatment, and has made a clear difference in survival

(Van Damme & Robberecht, 2009). Most of what we know about the pathogenesis of ALS comes from studies on the genetic forms. The significance of these monogenic forms in understanding the far more prevalent sporadic ALS is uncertain. Here, we will review some aspects of the current thinking on the etiology and pathogenesis of familial ALS and critically review its significance for the sporadic form of this dramatic motor neuron degeneration. Over the last two decades several genes, mutations in which cause ALS, have been identified (see Table 1). We here summarize what is known about the most common one of them. It should be noted that most of the mutations known to underly hereditary ALS have also been found in (a small set of) apparently sporadic ALS patients. Often selleck inhibitor (most of the time), it is uncertain whether these are really new mutants or

whether they have been misclassified as ‘sporadic’. This can happen in cases of non-paternity, in the presence of unknown, unreliable or incomplete family history, or if the parents of a patient are too young to draw conclusions, or have deceased before the age of penetrance of the phenotype. Incomplete penetrance, known to occur for some mutations, is another variable to take into account. Mutations in the SOD1 gene (chromosome 21) remain the most common cause of familial

ALS (Rosen et al., 1993). They are found in ∼20% of the families and thus account for ∼2% of all ALS. SOD1 is an enzyme of 153 amino acid residues, ubiquitously expressed and active as a homodimer. It catalyses the conversion of superoxide free radicals to hydrogen peroxide, which can be further Amino acid detoxified to water and oxygen by glutathione peroxidase or catalase. It should be distinguished from SOD2 (a mitochondrial SOD) and SOD3 (an extracellular SOD). Missense mutations, affecting almost every amino acid residue of the protein (and a few small deletions and insertions, in addition to rare C-terminal truncating non-sense mutations) are known to give rise to familial ALS, irrespective of their effect on dismutase activity (Borchelt et al., 1994; Robberecht et al., 1994; Rosen et al., 1994). Transgenic mice or rats overexpressing mutant SOD1 develop motor neuron degeneration with progressive muscle weakness, muscle wasting and reduced life span (Gurney et al., 1994; Ripps et al., 1995; Wong et al., 1995; Bruijn et al., 1997; Howland et al., 2002).

Taken together, the data suggest that c-fos expression in the POM modulates copulatory

behavior and sexual learning in male quail. “
“Whole-cell patch-clamp recordings of non-N-methyl-d-aspartate glutamatergic excitatory postsynaptic currents (EPSCs) were carried out from cholinergic neurons in slices of basal forebrain (BF) of developing rats aged 21–42 postnatal days to elucidate postnatal developmental change in Ca2+ channel subtypes involved in the transmission as well as that in dopamine D1-like receptor-mediated presynaptic inhibition. The amplitude of EPSCs was inhibited Selisistat supplier by bath application of ω-conotoxin GVIA (ω-CgTX; 3 μm) or ω-agatoxin-TK (ω-Aga-TK; 200 nm) throughout the age range examined, suggesting INNO-406 order that multiple types of Ca2+ channel are involved in the transmission. The EPSC fraction reduced by ω-CgTX decreased with age, whereas that reduced by ω-Aga-TK increased. Inhibition of the EPSCs by a D1-like receptor agonist, SKF 81297 (SKF; 30 μm) increased with age in parallel with the increase in ω-Aga-TK-induced inhibition. An activator of the adenylyl cyclase (AC) pathway, forskolin (FK; 10 μm) inhibited the EPSCs, and FK-induced inhibition also increased with age in parallel with the increase

in SKF-induced inhibition. Throughout the age range examined, SKF showed no further inhibitory effect on the EPSCs after ω-Aga-TK- or FK-induced effect had reached steady-state. These findings suggest that D1-like receptor-mediated presynaptic inhibition of glutamate release onto cholinergic BF neurons increases with age, and that the change is coupled with a developmental increase in the contribution

of P/Q-type Ca2+ channels as well as a developmental increase in AC pathway contribution. “
“Osteoarthritis is a degenerative joint disease associated with articular cartilage degradation. The major clinical outcome of osteoarthritis is a complex pain state that includes both nociceptive and neuropathic mechanisms. Currently, the therapeutic approaches for osteoarthritis are limited as no drugs are available to control the disease progression and the analgesic treatment has restricted efficacy. Increasing evidence from preclinical studies supports the interest of the endocannabinoid system as an emerging therapeutic target for osteoarthritis pain. Quinapyramine Indeed, pharmacological studies have shown the anti-nociceptive effects of cannabinoids in different rodent models of osteoarthritis, and compelling evidence suggests an active participation of the endocannabinoid system in the pathophysiology of this disease. The ubiquitous distribution of cannabinoid receptors, together with the physiological role of the endocannabinoid system in the regulation of pain, inflammation and even joint function further support the therapeutic interest of cannabinoids for osteoarthritis. However, limited clinical evidence has been provided to support this therapeutic use of cannabinoids, despite the promising preclinical data.

diphtheriae KCTC3075 has been characterized (Kim et al., 2010), which is the orthologue of DIP0543 C. diphtheriae NCTC SAHA HDAC purchase 13129 (Fig. 4), confirming that this organism has both normal sialidase but also a reported trans-sialidase activity (Mattos-Guaraldi et al., 1998). Other data suggested that C. diphtheriae harbours sialic acid on its cell envelope (Mattos-Guaraldi

et al., 1999). This could originate from the trans-sialidase activity moving sialic acid directly from host sialoglycans onto the bacterium’s surface. Both the lack of association of the sialidase with production of the diphtheria toxin (Warren & Spearing, 1963; Moriyama & Barksdale, 1967) and the lack of a need for uptake for cell surface modification were perhaps the reason why no study has ever examined the capability of C. diphtheriae to use sialic acid as a nutrient in vivo, which this study would suggest it is capable of. While the identity of a sialidase Smad3 signaling in C. diphtheriae has been known for

nearly 50 years, the presence of a sialidase in C. glutamicum has not been suspected. This enzyme is not orthologous to the sialidases seen in C. diphtheriae, C. ulcerans and C. pseudotuberculosis, but rather is most similar to Arthrobacter sp. The essential nature of the ABC transporter in the same gene cluster as the sialidase (cg2935) suggests that Cg2935 is a sialidase; however, this will need experimental confirmation. This study presents the first evidence for an active transporter for Neu5Ac in an actinobacterium and increases the range of bacteria that appear to use an ABC transporter for this purpose. Other bacteria where sialic acid transporters have been characterized use tripartite ATP-independent periplasmic (TRAP) transporters (Severi et al.,

2005; Mulligan et al., 2009, 2012; Chowdhury et al., 2012), classical secondary transporters of the these major facilitator superfamily (Martinez et al., 1995; Mulligan et al., 2012) or sodium solute symporter family (SSS) transporters (Severi et al., 2010), although perhaps significantly all these are Gram-negative bacteria. The only clear work on sialic acid transport in Gram-positives are from Streptococcus pneumoniae, which also uses an ABC transporter (Marion et al., 2011a, b). The reduced growth lag when cells are precultured in the presence of sialic acid suggests either the presence of a sialic acid-specific activator or the inactivation of a repressor. Given the presence of a GntR-family transcription factor in the cluster (cg2936), it is probable that the presence of Neu5Ac or one of its catabolic product acts as the ligand to cause depression of the cluster. The additional observation is that derepression by Neu5Ac is not seen in the presence of glucose, suggesting a catabolic repression-type mechanism is in operation. The mechanisms of catabolite repression are not well studied in C. glutamicum, and in many cases, different carbon sources are co-metabolized.

diphtheriae KCTC3075 has been characterized (Kim et al., 2010), which is the orthologue of DIP0543 C. diphtheriae NCTC Selleckchem Buparlisib 13129 (Fig. 4), confirming that this organism has both normal sialidase but also a reported trans-sialidase activity (Mattos-Guaraldi et al., 1998). Other data suggested that C. diphtheriae harbours sialic acid on its cell envelope (Mattos-Guaraldi

et al., 1999). This could originate from the trans-sialidase activity moving sialic acid directly from host sialoglycans onto the bacterium’s surface. Both the lack of association of the sialidase with production of the diphtheria toxin (Warren & Spearing, 1963; Moriyama & Barksdale, 1967) and the lack of a need for uptake for cell surface modification were perhaps the reason why no study has ever examined the capability of C. diphtheriae to use sialic acid as a nutrient in vivo, which this study would suggest it is capable of. While the identity of a sialidase selleck inhibitor in C. diphtheriae has been known for

nearly 50 years, the presence of a sialidase in C. glutamicum has not been suspected. This enzyme is not orthologous to the sialidases seen in C. diphtheriae, C. ulcerans and C. pseudotuberculosis, but rather is most similar to Arthrobacter sp. The essential nature of the ABC transporter in the same gene cluster as the sialidase (cg2935) suggests that Cg2935 is a sialidase; however, this will need experimental confirmation. This study presents the first evidence for an active transporter for Neu5Ac in an actinobacterium and increases the range of bacteria that appear to use an ABC transporter for this purpose. Other bacteria where sialic acid transporters have been characterized use tripartite ATP-independent periplasmic (TRAP) transporters (Severi et al.,

2005; Mulligan et al., 2009, 2012; Chowdhury et al., 2012), classical secondary transporters of the Exoribonuclease major facilitator superfamily (Martinez et al., 1995; Mulligan et al., 2012) or sodium solute symporter family (SSS) transporters (Severi et al., 2010), although perhaps significantly all these are Gram-negative bacteria. The only clear work on sialic acid transport in Gram-positives are from Streptococcus pneumoniae, which also uses an ABC transporter (Marion et al., 2011a, b). The reduced growth lag when cells are precultured in the presence of sialic acid suggests either the presence of a sialic acid-specific activator or the inactivation of a repressor. Given the presence of a GntR-family transcription factor in the cluster (cg2936), it is probable that the presence of Neu5Ac or one of its catabolic product acts as the ligand to cause depression of the cluster. The additional observation is that derepression by Neu5Ac is not seen in the presence of glucose, suggesting a catabolic repression-type mechanism is in operation. The mechanisms of catabolite repression are not well studied in C. glutamicum, and in many cases, different carbon sources are co-metabolized.

CF150 than on Pseudomonas sp. N9 at the highest cadmium concentration. “
“Reports that bacteria within the Firmicutes phylum, especially the species Faecalibacterium prausnitzii, are less abundant in Crohn’s disease (CD) patients and supernatants from cultures of this bacterium are anti-inflammatory prompted the investigation of the possible correlations between the abundance

of F. prausnitzii and the response to treatment in patients with gut diseases Afatinib order and healthy controls. In a randomized, double-blind trial, faeces were collected from healthy volunteers, and from patients with active CD, ulcerative colitis (UC) and irritable bowel syndrome before and after treatment. The levels of F. prausnitzii DNA in faecal suspensions were determined by PCR. Treatment by an elemental diet was

effective, resulting in decreases in both the Harvey and Bradshaw index (P<0.001) and the concentrations of serum C-reactive protein (P<0.05). The total levels of F. prausnitzii in faecal samples from CD patients at presentation were lower than those in the other groups both before and after the treatment. There was no correlation between F. prausnitzii abundance and the severity of CD before treatment. Clinical improvement unexpectedly correlated with a significant decrease in the abundance of F. prausnitzii, especially the this website A2-165 subgroup (P<0.05). Our data suggest that a paucity of F. prausnitzii in the gastrointestinal microbial communities is likely to be a minor aetiological factor in CD: recovery following elemental diet is attributed to lower levels of gut flora. "
“Vibrio owensii is a potential bacterial pathogen in marine aquaculture system. In this Thalidomide study, five lytic phages specific against Vibrio strain B8D, closely related to V. owensii, were

isolated from seawater of an abalone farm. The phages were characterized with respect to morphology, genome size, growth phenotype, as well as thermal, and pH stability. All phages were found to belong to the family Siphoviridae with long noncontractile tails and terminal fibers. Restriction analysis indicated that the five phages were dsDNA viruses with molecular weights ranging from c. 30 to 48 kb. One-step growth experiments revealed that the phages were heterogeneous in latent periods (10–70 min), rise periods (40–70 min), and burst sizes [23–331 plaque-forming units (PFU) per infected cell] at the same host strain. All phages were thermal stable and were tolerant to a wide range of pH. The results indicated that these phages could be potential candidates of a phage cocktail for biological control of V. owensii in aquaculture systems. “
“The conversion of branched-chain amino acids to branched-chain acids or alcohols is an important aspect of flavor in the food industry and is dependent on the Ehrlich pathway found in certain lactic acid bacteria.

A total of 599 and 604 patients received etravirine and placebo, respectively (median treatment duration 96.0 and 69.6 weeks, respectively). There was no significant difference between the treatment groups in the frequency of neuropsychiatric Navitoclax AEs. However, a significant difference in the frequency of rash was observed (20.5% vs. 11.8%, respectively; P < 0.0001); rash was generally mild

to moderate in severity; the rate of discontinuation because of rash was low (2.2% vs. 0% in the etravirine and placebo groups, respectively). The frequency of hepatic AEs was low and similar between the treatment groups (8.7% vs. 7.1%, respectively; P = 0.3370); hepatic enzyme levels did not increase over time. Lipid-related laboratory abnormalities and changes over time in lipid levels were generally comparable between treatment groups. Adjusting for treatment exposure, the frequency of AEs remained similar between treatment groups, with Rapamycin price the exception of rash [13.7 vs. 9.3 per 100 PYE; relative risk (95% confidence interval) 1.48 (1.02–1.95)]. The frequency of AEs of interest was generally

similar between the treatment groups, both overall and when adjusted for treatment exposure, with the exception of rash which was more frequent in the etravirine group. The nonnucleoside reverse transcriptase inhibitor (NNRTI) etravirine, which has activity against both wild-type HIV and NNRTI-resistant HIV mutants in vitro [1, 2], has demonstrated durable virological and immunological efficacy in treatment-experienced patients with NNRTI resistance in the phase III TMC125 DUET (Demonstrate Undetectable viral load in patients Experienced with ARV Therapy) trials [3, 4]. The overall safety profile of etravirine over 96 weeks, along with safety results in patients coinfected with hepatitis B and/or C virus, has previously been reported [4, 5]. Similar to results reported at week 48, etravirine displayed a tolerability profile at week 96 that was generally similar to that of placebo, with the

exception of rash, which occurred at a higher frequency in the etravirine group [4]. While overall safety data from the week 96 analysis have previously been reported science [4], there has been no analysis of the potential effect of differential treatment exposure on these findings. In addition, only minimal overall findings have been previously reported on adverse events (AEs) and laboratory abnormalities of interest. AEs of interest are those events thought to be potentially associated with the investigational compound or class, or with the relevant disease state, or that have been identified as important, based on data from earlier studies. They represent an emerging and ever more important aspect of the characterization of the safety profile of a compound during its development and post-marketing follow-up.

Protein concentrations were measured

using the Bradford method with bovine serum albumin as the standard (Bradford, 1976). Pi concentrations were determined using the molybdenum-blue method (Clesceri et al., 1989). Escherichia coli cells grown overnight on the 2 × YT medium with shaking at 37 °C were collected by centrifugation. The pellet was washed twice with Pi-free MOPS medium and resuspended in the same medium containing 2 mM glycerol-3-phosphate to an OD600 nm of 0.2. Samples taken from the cultures were centrifuged, and the supernatants Selleckchem ABT263 were assayed for Pi. The Pfam database (Finn et al., 2008) indicated that E. coli YjbB consists of two distinct segments (Fig. 1). The N-terminal half of YjbB contains hydrophobic amino acid Seliciclib mouse residues whose sequence is conserved among eukaryotic type II Na+/Pi cotransporters and is designated the Na+/Pi cotransporter domain (Pfam accession number PF02690). Most Na+/Pi cotransporter proteins consist of two

repeats of this domain. In fact, the N-terminal half of YjbB also consists of two repeats of the Na+/Pi cotransporter domain (41% identity over 135 amino acids and 32% identity over 126 amino acids, respectively). The C-terminal half of YjbB contains two repeats of a PhoU domain (Pfam accession number PF01895) (21% identity over 80 amino acids and 15% identity over 60 amino acids, respectively), although the homology was considered insignificant in the database. Similarly, PhoU proteins also consist of two copies of the PhoU domain that form three-helix bundles (Liu et al., 2005; Oganesyan et al., 2005). This analysis suggested that YjbB might be involved both in Pi transport and in the regulation of Pho regulon genes. PhoU negatively regulates the Pho regulon genes (Wanner, 1996). We have reported that a phoU mutant, MT29, accumulated 1000-fold higher levels of polyP than the wild type due to the constitutive expression of pstSCAB (Morohoshi et al., 2002). To test whether the overproduction of YjbB can compensate for the loss of PhoU function, we introduced yjbB on a multicopy plasmid (pMWyjbB) into MT29. MT29 carrying pMWyjbB

had significantly lower levels of polyP (Table 2). One possible explanation for the reduction of polyP by YjbB is that the PhoU domain of YjbB see more had compensated for the chromosomal phoU mutation as a multicopy suppressor and reduced the expression of the Pho regulon genes. Because the phoA gene (alkaline phosphatase) is also one of the Pho regulon genes, we measured the alkaline phosphatase activity of MT29 carrying pMWyjbB. Unexpectedly, the levels of alkaline phosphatase activity were still high in the transformant, but they were reduced when pMWphoU was introduced (Table 2). It therefore seemed unlikely that YjbB overproduction reduced the expression of the Pho regulon genes. In other words, the reduced levels of polyP may not be due to the suppression of the increased expression of the PstSCAB Pi uptake system.