The His tag-fused iphR gene was expressed in E. coli BL21(DE3) cells harboring pETiphR. Production of a ca. 28 kDa protein was observed by SDS-PAGE (Fig. 2a). This value is close to the predicted molecular mass of ht-IphR (Mr, 31243). Although a portion of ht-IphR appeared in an insoluble fraction, ht-IphR produced in a soluble fraction was purified to near homogeneity by Ni affinity chromatography. We first

tried to determine the oligomeric state of ht-IphR by gel filtration chromatography but failed to obtain an elution profile, probably because ht-IphR is prone to aggregation. Therefore, we performed in vitro cross-linking experiment (Fig. 2b). A major shifted band appeared buy Panobinostat at ca. 58 kDa in the cross-linked

samples, suggesting that ht-IphR dominantly Romidepsin research buy forms a homodimer in solution. Purified ht-IphR was used for EMSAs with DNA fragments containing the iphA promoter region (Fig. S1). The mobility of the IPH-87 fragment, which covered the positions −38 to +49 and conferred the IPA-inducible promoter activity to E6 cells, gave a retarded band, whereas no retardation was observed for the IPH-227 fragment covering the positions +10 to +236 (Fig. S1). The IPH-60 fragment covering −27 to +33 was also retarded, suggesting the importance of IR1 and/or IR2 sequences for the binding of IphR. To examine which inverted repeat sequence is necessary for the binding of IphR, competitive EMSAs of the binding of ht-IphR to the IPH-60 fragment were performed. When unlabeled competitor DNAs, the IPH-IR1 fragment containing IR1 (positions −27 to −1) and IPH-IR2 fragment containing

IR2 (−8 to +16) were added to the reaction mixture, no significant decrease in the retarded band was observed, whereas the addition of IPH-IR12 fragment containing both IR1 and IR2 (−27 to +16) resulted in the abolishment of the binding of ht-IphR (Fig. S1). Therefore, we constructed the IPH-IR1H2 fragment containing IR1 and the upstream half-site of IR2 (−27 to +4), and the IPH-IR2H1 fragment containing IR2 and the downstream half-site of IR1 (−14 to +16). Only the GPX6 addition of IPH-IR2H1 into the EMSA of the binding of ht-IphR to the IPH-60 fragment caused a significant reduction of the retarded band. This suggests that both IR2 and the downstream half-site of IR1 are involved in the IphR binding. To examine which sequence is truly required for the binding of IphR, we prepared the mutated IPH-IR12 fragments in which the upstream half-site of IR1 (IPH-mutA), downstream half-site of IR1 (IPH-mutB), upstream half-site of IR2 (IPH-mutC), and downstream half-site of IR2 (IPH-mutD), were mutated as indicated in Fig. 3a. EMSAs of the binding of various concentrations of ht-IphR to these mutated IPH-IR12 fragments showed the formation of IphR-DNA complex when the IPH-mutA fragment was used as a probe (Fig. 3b).

l-methionine, l-leucine, l-isoleucine and l-threonine were found to be catalysed by the investigated enzymes, producing l-methionine sulfoxide, 4-hydroxyleucine, 4-hydroxyisoleucine and 4-hydroxythreonine, respectively. An investigation of enzyme kinetics suggested the existence of a novel subfamily of bacterial dioxygenases within the PF10014 family MLN0128 manufacturer for which free l-amino acids could be accepted as in vivo substrates. A hypothesis regarding the physiological significance of hydroxylated l-amino acids is also discussed. Hydroxylation of

free canonical l-amino acids is an interesting and growing field of biotechnology and molecular biology research. Introduction of a functional hydroxyl group into amino acid molecules makes possible synthesis of fine chemicals (Blaskovich et al., 1998). In addition, the hydroxylated amino acid may itself be biologically active with pharmacological significance (Jette et al., 2009) and/or may be involved in bacterial metabolic regulation (Ogawa et al., 2011). In bacteria, the hydroxylation of free l-amino acids

learn more is usually catalysed by specific Fe(II)/α-ketoglutarate-dependent dioxygenases (Hausinger, 2004). Because both l-amino acids and α-ketoglutarate are involved in cell metabolism, metabolic engineering of Escherichia coli could be used for the microbiological production of target hydroxylated l-amino acids (Shibasaki selleck chemical et al., 2000; Smirnov et al., 2010; Ogawa et al., 2011).[ Correction added after online publication 17 April 2012: Kim et al., 2010 and Smirnov et al., 2010 references swapped throughout ]. Thus, identification of novel l-amino acid dioxygenases or l-amino acid hydroxylation activities may facilitate industrial bioprocesses

to produce novel pharmaceuticals and synthons for organic chemistry. In addition, understanding the hydroxylation of free l-amino acids could facilitate the discovery of novel biosynthetic processes and regulatory mechanisms in bacteria. Recently, we described the cloning and characterization of l-isoleucine-4-hydroxylase (IDO) from Bacillus thuringiensis (Kodera et al., 2009; Smirnov et al., 2010; Hibi et al., 2011; Ogawa et al., 2011). IDO hydroxylated several hydrophobic aliphatic l-amino acids, including l-leucine, and generated l-methionine sulfoxide from l-methionine. In this work, we used IDO homologues from several bacteria to examine the substrate specificities of novel dioxygenases in regard to other canonical l-amino acids and to determine kinetic constants for l-isoleucine, l-leucine and l-methionine. To construct the pET-HT-IDO, pET-HT-PAA, pET-HT-MFL and pET-HT-GOX plasmids, the following DNA fragments were amplified: (1) a 776-bp ‘IDO’ fragment, using the primers svs 335 (5′-TATACCATGGGCAGCAGCCATCATCATCATCATCACAGCAGCGGCAAAATGAGTGGCTTTAGCATAGAAGA-3′) and svs 336 (5′-CAGCCGGATCCTTATTTTGTCTCCTTATAA-3′) and the pEL-IDO plasmid (Smirnov et al.

4. Samples were examined in a Tecnai 12 BioTWIN (FEI, Eindhoven, the Netherlands) operated at 120 kV. For scanning electron microscopy, substrates were removed from the serum bottles JQ1 molecular weight and washed twice for 15 min in medium. Samples were then fixed with 2% glutaraldehyde

in 100 mM sodium phosphate buffer containing 2% NaCl for 30 min at room temperature. The samples were then taken through a series of ethanol dehydration steps (25%, 50%, 70%, 90% and 100% ethanol) for 15 min each, followed by hexamethyl-disilazane. Dried specimens were mounted on aluminum stubs, sputter coated with approximately 2 nm of gold/palladium and examined in a JEOL JSM-7500F scanning electron microscope. Methanococcus maripaludis possesses two surface appendages, flagella and pili, which could both potentially be involved in attachment of cells in

the environment. To investigate the role of these appendages in attachment, mutants that lacked one or the other, or both, appendages were generated. The nonflagellated, but piliated mutant in the preflagellin peptidase flaK has been described previously (Ng et al., 2009). To create mutant strains that lacked pili, the eppA gene, the prepilin Epacadostat peptidase necessary for the removal of the signal peptide from pilins, was targeted. This would be predicted to prevent the incorporation of the nonprocessed pilins into pili fibers, leading to nonpiliated cells (Strom & Lory, 1993). If this gene is knocked out in the wild-type background, then cells should be flagellated, but nonpiliated. Mutants deleted for eppA were readily isolated and identified by a PCR screen (Fig. 1). Examination by TEM demonstrated that these mutants were, as predicted, flagellated (approximately 12 nm diameter fibers), but nonpiliated (Fig. 2). If eppA is deleted in the flaK mutant background, then such double-deletion see more mutants should lack both flagella due to the loss of flaK and also pili due to the deletion of eppA. Such mutants were readily isolated and identified by PCR screening (Fig. 1). Examination of the double deletion

strains indicated that the cells did lack both surface appendages (Fig. 2). Complementation of the eppA deletion strain with a plasmid copy of the gene restored the piliated state (data not shown). Wild-type cells synthesized both appendages while the previously reported flaK mutant was nonflagellated, but piliated (approximately 6 nm diameter fibers) (Fig. 2). The four strains were examined for their ability to attach to a variety of available substrates. Substrates tested included numerous uncoated electron microscopy grid types, as well as glass, mica and silicon wafer chips. After 24 h, wild-type cells were shown to attach to varying degrees to all surfaces tested, except mica (Fig. 3 for molybdenum grids and silicon chips; others not shown), although the number of cells attached to glass were few. Cells often preferred the edges of grids, where the rough surface seemed favorable for attachment (Fig. 3a).

GPP 8.2.3.2 ● We recommend if patients are commencing ART, and DAAs are not being considered, standard first-line ART should be commenced. GPP   ● We recommend when DAAs are to be used there is careful consideration of possible DDIs (1C) and current or archived HIV resistance. All drug interactions should be checked with an expert source (e.g., www.hiv-druginteractions.org).     ● We recommend if boceprevir is to be used, RAL with TDF plus FTC should be the treatment of choice for those with wild-type HIV (1C): pharmacokinetic data would support

ETV, RPV and MVC as alternatives.     ● We recommend if telaprevir is to be used either RAL or standard-dose ATV/r should Talazoparib be used (1C): pharmacokinetic data would support ETV, RPV and MVC as alternatives. EFV may be used but the telaprevir dose needs to be increased to 1125 mg tds.     ● We suggest that if ABC is to be used with ribavirin, the ribavirin should be weight-based dose-adjusted. 2C 8.3.1 We recommend starting ART in HIV-positive patients with KS. 1A   We recommend starting ART in HIV-positive patients with non-Hodgkin lymphoma (NHL). 1B   We suggest starting ART in HIV-positive patients with cervical

cancer. 1C   We recommend starting ART in HIV-positive patients who are commencing radiotherapy or chemotherapy Selleckchem 3-MA for cervical cancer. 1D 8.3.2 We suggest starting ART in HIV-positive patients with non-AIDS-defining malignancies (NADMs). 2C   We recommend starting ART in HIV-positive patients who are commencing immunosuppressive radiotherapy or chemotherapy for NADMs. 1C 8.3.3 We recommend that potential

pharmacokinetic interactions between ARVs and systemic anticancer therapy be checked before administration (with tools such as: http://www.hiv-druginteractions.org). GPP   We suggest avoiding ritonavir-boosted ART in HIV-positive patients who are to receive cytotoxic chemotherapy agents that are metabolized by the cytochrome P450 (CYP450) enzyme system. 2C   We recommend against the use of ATV in HIV-positive patients who are to receive irinotecan. 1C   We suggest avoiding ARV agents in HIV-positive patients who are to receive cytotoxic chemotherapy agents that have overlapping toxicities. 2C 8.4.2 We recommend patients with symptomatic HIV-associated NC disorders Dapagliflozin start ART irrespective of CD4 lymphocyte count. 1C 8.4.3 We recommend patients with HIV-associated NC disorders start standard combination ART regimens. 1C 8.4.4 In patients with ongoing or worsening NC impairment despite ART we recommend the following best practice management: GPP ● Reassessment for confounding conditions. ● Assessment of cerebrospinal fluid (CSF) HIV RNA, CSF HIV genotropism and genotyping of CSF HIV RNA. ● In subjects with detectable CSF HIV RNA, modifications to ART should be based on plasma and CSF genotypic and genotropism results. 8.5.1 We recommend patients with HIVAN start ART immediately irrespective of CD4 cell count.

Biodegradation of petroleum hydrocarbons in marine and freshwater environments is constrained by the ability of microorganisms to access the hydrophobic surfaces of oil droplets. A key process for attachment to oil droplets involves the production of surface active agents (Horowitz et al., 1975), which is further accompanied by changes in the properties of the cell envelope. One of the most notable features is the formation of canals in the cell wall, which appears to enable the

transport of nanometer-sized droplets into the surface of the interior cell membrane (Southam et al., 2001). The first step involving the secretion of surface active agents includes the production of relatively low-molecular-weight

surfactants that decrease the surface tension and excretion of Vorinostat mw high-molecular-weight polysaccharide polymers that serve to emulsify the oil and water into small particles that provide increased surface area for enzymatic attack. In several studies, these exopolymers appear along with fibrils and wall appendages (Marin et al., 1996; Macedo et al., 2005), and can include embedded flagella that are used for both motility and attachment of the cells to the oil surface (Marin et al., 1996). Another microscopic study further reports the appearance of cellular aggregates that form over the surface Ganetespib cell line of oil droplets and invade the oil as the biofilm matures (Macedo et al., 2005). Altogether, these studies provide the basis for comparisons of different model systems. On the other hand, there have been Non-specific serine/threonine protein kinase few comparative studies examining different microorganism and substrate conditions using the same methods. Moreover, the three-dimensional (3D)

structures of the microhabitats that are generated by exocellular polymers have not yet been described using 3D reconstructions of serial sections cut through oil droplets that are colonized by microorganisms. With the current interest in the remediation of oil-polluted marine and freshwater environments, a better description of the feeding structures is highly relevant for understanding how biophysical processes and cell wall adaptations influence the rate of oil degradation. The research described here used a combination of cytochemical stains and microscopy techniques to describe the specific exocellular fibrils, films and internal granules that are generated by yeasts and bacteria during oil droplet colonization. A novel aspect of the present research was the use of serial sections and computer imaging to generate a 3D reconstruction of the habitat that is formed by selected yeast and bacteria on the oil droplet surfaces. These trophic structures appear as pits and cavities that enclose microbial cells along with the polymers and enzymes that are produced by the oil-degrading microorganisms.

1a) and the observed abnormal (or

small) stem growth in the clinostat-cultured mushrooms Lentinus tigrinus and P. brumalis (Moore, 1991; Gorovoj Obeticholic Acid et al., 1989). In conclusion, the products of the differentially expressed genes affected by clinostat rotation (i.e. under simulated microgravity environment) consist of various putative proteins that are likely to be involved in cellular activities in general metabolic activities, cell structure, and responses to stresses. Indeed, we found several proteins that were apparently involved in fruiting body formation. Since writing up this study, comprehensive analyses of differentially expressed genes or proteins under simulated microgravity have been reported in mammals (Clement et al., 2007; Patel et al., 2007; Sarkar et al., 2006), plants (Barjaktarovićet al., 2007; Wang et al., 2006), insects (Marco et al., 2007), yeasts (Sheehan et al., 2007), and bacteria (Nickerson et al., 2003). However, almost all the studies on the response of microorganisms to gravity have been carried out

on unicellular organisms. Moreover, unlike the cells of higher animals and plants, almost every cell of the mushroom can function as a ‘stem cell’ (Money, 2002). The mushroom can be considered a multicellular signaling pathway model organism for physiological experiments on changes in environmental factors such as the gravity and other stresses. Experiments using mushrooms, including P. ostreatus, will provide more information required to clarify the cellular responses involved in gravitropism, especially in the morphological development of fruiting bodies. This work was partly supported by a Grant-in-Aid for Scientific Sirolimus datasheet Research (No. 17780068) from the Ministry of Education, Culture, Sports, Science, and Technology of Japan. “
“The use of natural compounds as inhibitory agents for virulence factor production is a new approach to overcome increased antimicrobial resistance in pathogenic bacteria. In this study, we examined whether red chilli (Capsicum annuum) contains any such compound(s) that can repress the cholera

toxin (CT) production in Vibrio cholerae. We found that the methanol extract of red chilli could inhibit CT production in recently emerged V. cholerae O1 El Tor variant strains without affecting their viability. Interestingly, capsaicin, a well-studied active component of red chilli, also drastically inhibited CT production in V. cholerae strains belonging to various serogroups including variants. Real-time quantitative reverse transcription-PCR assay revealed that capsaicin effectively repressed the transcription of ctxA, tcpA and toxT genes, but not of toxR and toxS genes. On the contrary, capsaicin significantly enhanced the transcription of the hns gene, the product of which is known to regulate negatively the transcription of ctxAB, tcpA and toxT genes.

UniFrac distances ranged from 0.298 to 0.607 and were higher between the initial and late stage samples. UniFrac tests have been previously used as a semi-quantitative determination of the similarities between the bacterial communities on the phyllosphere of Populus deltoides sampled at different times (Redford et al., 2010). According to our estimations, major changes

in the phenol-degrading bacterial community may occur between the initial and midterm stages of leaf decomposition. At the midterm, the greatest community richness and diversity was found and coincided with increasing phenol selleck kinase inhibitor oxidase activity and maximum fungal biomass (Artigas et al., 2011). The LmPH sequences from this stage were scattered throughout the phylogenetic tree (in clusters A, B, C, and E), and their corresponding enzymes exhibit different kinetic properties. AZD2281 mw It is known that bacteria and fungi have complementary roles in leaf litter degradation. Bacteria are thought to increase their contribution only after leaf material has been partially broken down (Baldy et al., 1995), whereas fungi, especially

aquatic hyphomycetes, have been recognized as dominant, in terms of both activity and biomass, during early decomposition (Gulis & Suberkropp, 2003; Romaní et al., 2006). However, bacteria may make a greater contribution to leaf litter decomposition particularly when fungal activity is compromised by unfavorable conditions (Pascoal & Cassio, 2004; Kubartova et al., 2009). In conclusion, by analyzing the LmPH gene from different leaf decomposition stages, we have shown that the bacterial community changes significantly over the course of leaf litter degradation in streams. During Adenosine triphosphate early decomposition, the bacterial community is rather complex and potentially exhibits a low degree of metabolic

specialization in view of the deduced enzyme kinetics. As decomposition progresses, the phenol-degrading bacterial community is dominated by suspected low-Ks type bacteria, with a high similarity to Alcaligenes spp., Comamonas sp., and Ralstonia sp, suggesting a gradual selection of specialized phenol degraders as decomposition progressed. To the best of our knowledge, this work represents the first specific analysis of any functional gene marker and of bacterial and fungal origin, used for investigating microbial communities during the leaf litter decomposition process in streams. Time series analyses of bacterial and fungal communities in leaf litter decomposition have previously been performed using either DGGE or terminal-restriction fragment length polymorphism (T-RFLP) of amplified SSU rRNA fragments (Das et al., 2007; Marks et al., 2009; Kelly et al., 2010), although no general conclusions can be derived from these studies. The relative presence of general and specialized microorganisms on leaf surfaces during litter decomposition has been proposed as a major determinant of diversity (Das et al., 2007).

Assessments of liver function (LFTs) should include ALT and/or AST, ALP, GGT, bilirubin and albumin, and should be performed at baseline, routine clinic visits and during illness (IIa). More frequent monitoring is recommended during the first 3 months of exposure to (new) antiretrovirals (except nevirapine; see below), at approximately 1 month and 3 months (III). More frequent monitoring of LFTs (every 2 weeks during the first 2 months of treatment, at the third month, and then regularly thereafter) is recommended in the summary of product characteristics (SPC) for nevirapine. Patients with persistently raised markers of liver injury Src inhibitor or

newly occurring abnormal liver tests should be investigated for viral hepatitis, opportunistic infection, malignancy, drug toxicity or fatty liver disease (IIa). Sporadic high ALT levels are common. Apparent elevations should be confirmed (III). Acute hepatitis C should be excluded if an appropriate exposure history is obtained. Kidney disease may affect up to 30% of HIV-infected patients. Acute renal Forskolin manufacturer failure is largely restricted

to hospitalized patients with infection, liver disease or malignancy [4]. Chronic kidney disease (CKD) is associated with advanced HIV infection, older age, diabetes mellitus, hypertension and use of indinavir or tenofovir [5, 6]. In Black patients, HIV-associated nephropathy (HIVAN) is an important cause of CKD and typically presents with heavy proteinuria and advanced renal failure at HIV diagnosis [7]. In other ethnicities, most CKD is associated with metabolic, vascular or urological disease, and drug toxicity [6]. The prognosis of Black patients with HIV-associated

chronic kidney disease has improved dramatically in the HAART era, and the number of patients requiring long-term renal replacement has risen considerably in recent years [8]. CKD may be diagnosed by the presence of haematuria, proteinuria or reduced estimated glomerular filtration rate (eGFR) for more than 3 months [9]. Use of creatine supplements as a possible explanation for raised serum creatinine levels (and reduced eGFR) should be excluded. Proteinuria is a risk factor for developing renal failure [10] and (cardiovascular) death [11]. Patients with severe renal impairment, progressive decline in renal function, persistent haematuria or significant proteinuria Methane monooxygenase (above 500 mg/24 h) should be investigated to establish the aetiology. ART may slow the progression of CKD, at least in patients with HIVAN [12, 13]. Although most antiretroviral drugs may cause renal injury, indinavir and tenofovir have been most frequently associated with nephrotoxicity [14]. Crystallization of indinavir in the urinary tract may result in nephrolithiasis or tubulo-interstitial nephritis. Most episodes resolve with rehydration and drug discontinuation, although gradual loss of renal function and progressive or irreversible renal failure have also been reported [14].

, 2000). In sialic acid

detection, only types 1, 1/2, 2, 14, 15, and 16 agglutinated with lectin (Charland et al., 1995). CPS of serotypes 1, 2, 14, 16 and 1/2 was predicted to contain sialic acid, which can enhance intracellular survival, participate in biofilm formation, or mask this website underlying antibody epitopes (Severi et al., 2007). The cps10 locus contains the putative glycerol phosphotransferase gene (wcxP). Serotype 10 CPS may be composed of glycosylglycerol repeating unit, which exists in the CPS of other microorganisms (Altman et al., 1987a, b; Beynon et al., 1991). The metalloprotease (wcyI) and pyruvyltransferase (whaL) was only found in serotypes 7 and 23, respectively. Pyruvyltransferase is identified as an enzyme which can transfer pyruvate substitutions into CPS saccharide intermediates (Lew & Heidelberger, 1976; Kim et al., 2002). The function of metalloprotease in the cps7 locus is unknown. Nucleotidyltransferases are contained in the cps locus of serotypes 3 and 9. Putative LicD-family phosphotransferases LGK 974 are contained in the locus of serotypes 8, 9 and 25. There are one-way or two-way cross-reactions in some S. suis serotypes. Two-way cross-reactions between serotypes 1/2 and 1, and serotypes 1/2 and 2 were detected. A one-way cross-reaction was detected between types 1 and 14 (Higgins & Gottschalk,

1990). The comparison results showed that the cps loci of serotypes 1, 2, 14 and 1/2 are similar (Fig. 2). With the exception of serotype 1/2, the serotypes can infect not only pigs but also humans, and can cause disease and/or death (Heath et al., 1996; Vilaichone et al., 2002; Haleis et al., 2009; Kerdsin et al., 2009; Gottschalk et al., 2010). The similar CPS production was predicted to be one of the reasons for the high pathogenicity of the three serotypes. The cpsK-T fragments of all four serotypes are highly similar. The cpsE–J fragments of serotypes 1 and 14 are similar, but are different

from that of serotypes 2 and 1/2. The cpsE-J fragments of serotypes 2 and 1/2 are also similar. The PtdIns(3,4)P2 serotype 1 cps locus lacks a 906-bp fragment containing IS630-Spn1 transposase in the S. suis serotype 2 cps locus, resulting in the earlier transcription termination of the cps locus. The same fragment is contained in the serotype 14 cps locus at a similar position, with the addition of one base. A reversed sequence of the same fragment is contained in the serotype 1/2 cps locus, which results in IS630-Spn1 being changed into IS66-Spn1 transposase. The critical difference between the serotype 1 and 14 loci or the serotype 2 and 1/2 loci is a 906-bp fragment containing IS transposase. The cps locus of the four serotypes appears to have evolved from the same ancestor. They could be stable binary transformants produced by homologous recombination.

, 2000). In sialic acid

detection, only types 1, 1/2, 2, 14, 15, and 16 agglutinated with lectin (Charland et al., 1995). CPS of serotypes 1, 2, 14, 16 and 1/2 was predicted to contain sialic acid, which can enhance intracellular survival, participate in biofilm formation, or mask DZNeP supplier underlying antibody epitopes (Severi et al., 2007). The cps10 locus contains the putative glycerol phosphotransferase gene (wcxP). Serotype 10 CPS may be composed of glycosylglycerol repeating unit, which exists in the CPS of other microorganisms (Altman et al., 1987a, b; Beynon et al., 1991). The metalloprotease (wcyI) and pyruvyltransferase (whaL) was only found in serotypes 7 and 23, respectively. Pyruvyltransferase is identified as an enzyme which can transfer pyruvate substitutions into CPS saccharide intermediates (Lew & Heidelberger, 1976; Kim et al., 2002). The function of metalloprotease in the cps7 locus is unknown. Nucleotidyltransferases are contained in the cps locus of serotypes 3 and 9. Putative LicD-family phosphotransferases Selleck Dasatinib are contained in the locus of serotypes 8, 9 and 25. There are one-way or two-way cross-reactions in some S. suis serotypes. Two-way cross-reactions between serotypes 1/2 and 1, and serotypes 1/2 and 2 were detected. A one-way cross-reaction was detected between types 1 and 14 (Higgins & Gottschalk,

1990). The comparison results showed that the cps loci of serotypes 1, 2, 14 and 1/2 are similar (Fig. 2). With the exception of serotype 1/2, the serotypes can infect not only pigs but also humans, and can cause disease and/or death (Heath et al., 1996; Vilaichone et al., 2002; Haleis et al., 2009; Kerdsin et al., 2009; Gottschalk et al., 2010). The similar CPS production was predicted to be one of the reasons for the high pathogenicity of the three serotypes. The cpsK-T fragments of all four serotypes are highly similar. The cpsE–J fragments of serotypes 1 and 14 are similar, but are different

from that of serotypes 2 and 1/2. The cpsE-J fragments of serotypes 2 and 1/2 are also similar. The 5-FU order serotype 1 cps locus lacks a 906-bp fragment containing IS630-Spn1 transposase in the S. suis serotype 2 cps locus, resulting in the earlier transcription termination of the cps locus. The same fragment is contained in the serotype 14 cps locus at a similar position, with the addition of one base. A reversed sequence of the same fragment is contained in the serotype 1/2 cps locus, which results in IS630-Spn1 being changed into IS66-Spn1 transposase. The critical difference between the serotype 1 and 14 loci or the serotype 2 and 1/2 loci is a 906-bp fragment containing IS transposase. The cps locus of the four serotypes appears to have evolved from the same ancestor. They could be stable binary transformants produced by homologous recombination.