Environments faced by soil rhizobia range from a rhizosphere rich in nutrients and root exudates, to soils deficient in nitrogen, phosphates, water, and nutrients. Numerous microbial species, including rhizobia, form microcolonies or biofilms when they colonize roots. Available data on surface attachment and/or biofilm formation by rhizobia are summarized in Table 1. Biofilm formation allows non-spore-forming soil bacteria to colonize surrounding habitat, and to survive common environmental stresses such as desiccation and nutrient limitation. The biofilm mode of life is often crucial for survival of bacteria, as well as for establishment Smad inhibitor of symbiosis with the

legume host. Biofilm formation is believed to occur as a sequential developmental process, culminating in the selleck kinase inhibitor establishment of these bacterial communities (Fig. 1). Still, an integrated view of biofilm formation in rhizobia has not been presented. In order to organize available information in this review,

data are summarized for each of the four major genera: Mesorhizobium, Sinorhizobium, Bradyrhizobium, and Rhizobium. Biofilm formation has been reported in two Mesorhizobium species, Mesorhizobium huakuii and Mesorhizobium tianshanense (Wang et al., 2004, 2008), which, like all members of this genus, show a growth rate intermediate between those described for Rhizobium and Bradyrhizobium. Quorum sensing is a mechanism allowing bacteria to sense population density and regulate gene expression, leading to activation of specific phenotypes in the population. The process depends on the accumulation in the environment of a signaling molecule termed autoinducer. Many Gram-negative bacteria use N-acylhomoserine lactones (AHLs) as signal molecules, and some have been reported to use other fatty acid derivatives such as 3-hydroxypalmitic acid methyl ester and cis-unsaturated fatty acids. In contrast, many Gram-positive bacteria

use amino acids or modified peptides as signal molecules. Both Gram-positive and Gram-negative bacteria use isomers of methyl-2,3,3,4-tetrahydroxytetrahydrofuran (the AI-2 autoinducer) as signals. Signal molecules belonging Ribose-5-phosphate isomerase to other structural classes (indole and its derivatives, quinolones, and (S)-3-hydroxytridecan-4-one) have also been described (Ryan & Dow, 2008). The production of these autoinducers has been described for M. huakuii, which establishes a symbiotic relationship with Chinese milk vetch, Astragalus sinicus (Zhu et al., 2003). Overexpression of the A. tumefaciens quorum regulator TraR in M. huakuii strain Mh93 interfered with the endogenous quorum-sensing system, probably because of competitive binding of TraR proteins to rhizobia AHLs (Wang et al., 2004). A strain overexpressing TraR formed thinner biofilms than the control strain, suggesting that quorum sensing positively regulates biofilm formation in M. huakuii (Wang et al., 2004). Production of AHLs has also been described for M.

Fluoroquinolones must enter the cell to become effective; therefore, the properties of the cell surface properties play an essential role in the determination of antimicrobial resistance. Electrostatic interactions

between negatively charged bacteria and EuCl-OFX (positive zeta Cobimetinib in vitro potential) put them in touch quickly and reverse the bacterial surface charge. EuCl-OFX has a strong OM-permeabilizing activity at concentrations below the levels needed to achieve eradication of inocula after brief exposure (sub-MIC concentrations of OFX). Although there are reports of OM-permeabilizing action for some fluoroquinolones, it arises as a side effect and occurs after prolonged exposure to supra-MIC concentrations (Chapman & Georgopapadakou, 1988; Vaara, 1992; Mason et al., 1995). Moreover, a previous report showing that

ofloxacin Selleck 5FU does not sensitize P. aeruginosa to hydrophobic antibiotics (Vaara, 1992) contributes to our results, attributing the observed effect to the action of cationic polymer. EuCl-OFX interacts with both bacterial cell membranes. In addition to the OM permeabilization, EuCl-OFX causes concentration-dependent depolarization of cytoplasmic membrane in P. aeruginosa cells. The alterations in the bacterial envelopes are reflected in the changes observed in size and granularity of the bacterial cell. Drug-free polymer exhibited bacteriostatic or weakly bactericidal effect after a short exposure time and subsequently recovered. According to the performance of Farnesyltransferase other known polycationic permeabilizers (Vaara, 1992), our results indicate that, to a large extent and despite being a powerful permeabilizer, EuCl does not kill P. aeruginosa. This lack of correlation between cytoplasmic membrane depolarization and bacterial cell lethality was also described for cationic antibacterial peptides (Zhang et al., 2000). The inhibition of P. aeruginosa growth by EuCl-OFX may involve surface effect and, to some extent,

permeation effect. The cationic polymer would mitigate the electronegativity of cell surface in the process of disorganizing the OM, rendering it permeable to antibiotic. In addition, cytoplasmic membrane depolarization turns bacterial cell more vulnerable. Therefore, the bactericidal action exhibited by EuCl-OFX is derived from a mechanism combining OM-permeabilization and bacterial membrane depolarization coupled with the action of fluoroquinolones on intracellular target. To our knowledge, this is the first study on the interaction of Eudragit E100® with bacterial cells. Although Eudragit E100® is not bactericidal in itself, the ability to alter the OM of P. aeruginosa and induce changes in membrane potential extends the applicability of this polymer as a vehicle for drug delivery into cells or as an adjuvant or potentiator for fluoroquinolones in topical pharmaceutical preparations.

For the plus-enzyme control, an UMP assay was performed in the absence of inhibitor. In the minus-enzyme control, sterile water instead of enzyme was used. The IC50s were calculated using a linear regression standard curve to predict the concentration of compound needed for 50% inhibition. One unit of activity was defined as the amount of enzyme required to degrade 0.1 nmol of ATP in Roxadustat cell line 120 min at 30 °C under the conditions described above. The minimum inhibitory concentrations (MICs) were determined by a standard microdilution broth method (National Committee for Clinical Laboratory Standards, 2003) with slight modifications. Briefly, the inoculum

size was ~5 × 105 CFU mL−1 in the final assay volume of 50 μL. The microdilution plates inoculated with bacteria were incubated at 35 °C for 18–20 h, and

the MIC was determined as the lowest concentration of the compound that completely inhibited the viable growth of the organism in the microdilution wells. Equilibrium analysis by SPR was performed using a Biacore3000 and the CM5 sensor chip (GE Healthcare INK 128 research buy Japan). SpPyrH was covalently coupled to CM5 using a standard amine coupling method according to the manufacturer’s protocol. Briefly, CM5 was activated by injecting a mixture of 20 mM N-hydroxysuccinimide (NHS) and 80 mM 1-ethyl-3- (3-diethylaminopropyl) carbodiimide hydrochloride. After being diluted tenfold with acetate buffer (pH 4.8), SpPyrH (0.1 mg mL−1) was injected at 10 μL min−1 for 7 min and then CM5 was inactivated by 1 M ethanolamine hydrochloride

(pH 8.5) to block the residual NHS ester groups. Running buffer (10 mM Hepes (pH7.4), 150 mM NaCl, 3 mM EDTA, 0.005% Surfactant (GE Healthcare Japan), 5% DMSO) was used in all binding experiments. All compounds dissolved in DMSO were diluted 1 : 20 with the running buffer without 5% DMSO. The samples were injected at 30 μL min−1 check for 2 min. The response was measured in resonance units (RU), and data analysis of the sensorgrams was performed using BIAevaluation software ver. 3.1 and the response at the equilibrium phase of interaction was obtained using the software program ‘equilibrium analysis model’. To obtain recombinant PyrH proteins, the SpPyrH or HiPyrH, each tagged with 6xHis at NH2-terminus, was expressed in E. coli and then purified using the Ni-affinity resin. When purified SpPyrH or HiPyrH protein was examined by SDS–PAGE followed by Coomassie staining, a prominent band was detected of 29.2 or 28.3 kDa in size, respectively, which was deduced as the molecular weight of SpPyrH or HiPyrH (Fig. 1a and c). These proteins were also detected by Western blotting analysis with anti-6xHis antibody, suggesting that each of these proteins is an authentic target protein (Fig. 1b and d).

This research was supported selleck by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2011-0003256). “
“Both ThyA and ThyX proteins catalyze the transfer of the methyl group from methylenetetrahydrofolate (CH2H4-folate) to dUMP, forming dTMP. To estimate the relative steady state expression levels of ThyA and ThyX, Western blot analysis was performed using ThyA or ThyX antiserum on total protein from the wild-type, ΔthyX, and thyX-complemented strains of Corynebacterium glutamicum.

The level of ThyA decreased gradually during the stationary growth phase but that of ThyX was maintained steadily. Whereas the expression level of ThyA in a ΔsigB strain was comparable to that of the wild-type,

the level of ThyX was significantly diminished in the deletion mutant and was restored to that of the wild-type in the complemented strain, indicating that the level of ThyX was regulated by SigB. Growth of the C. glutamicum ΔsigB strain was dependent upon coupling activity of dihydrofolate reductase (DHFR) with ThyA for the synthesis of thymidine, and thus showed sensitivity to the inhibition of DHFR by the experimental inhibitor, WR99210-HCl. These results suggested that the relative levels of ThyA and ThyX differ in response to different growth phases and that SigB is necessary for maintenance PD-0332991 in vitro of the level of ThyX during transition into the stationary growth phase. dTMP is a key metabolite required for the biosynthesis of dTTP, a building block of DNA. The enzymes thymidylate synthase ThyA (EC 2.1.1.45) and ThyX (EC 2.1.1.148) can each catalyze the de novo formation

of dTMP in vivo. Both ThyA and ThyX proteins catalyze Chloroambucil the transfer of the methyl group from CH2H4-folate to dUMP, forming dTMP. The homodimeric ThyA protein carries out reductive methylation of dUMP, using CH2H4-folate as a reductant and the source of a methylene group, generating dTMP and dihydrofolate (H2-folate). As reduced folates are essential for many biochemical processes, H2-folate is reduced to tetrahydrofolate (H4-folate) by dihydrofolate reductase (DHFR) with subsequent regeneration of CH2H4-folate, catalyzed by serine hydroxymethyltransferase. In contrast, the homotetrameric ThyX protein utilizes CH2H4-folate solely as a one-carbon donor and uses Flavin Adenine Dinucleotide (FAD)-mediated hydride transfer for the reduction of the methylene to form dTMP and H4-folate (Giladi et al., 2002; Graziani et al., 2004; Griffin et al., 2005; Koehn et al., 2009; Leduc et al., 2003, 2007; Liu & Yang, 2004; Myllykallio et al., 2002, 2003; Sampathkumar et al., 2005; Zhong et al., 2006). Corynebacterium glutamicum ATCC 13032 is a non-sporulating and non-pathogenic soil bacterium belonging to the group of high G + C Gram-positive Actinobacteria (Hecht & Causey, 1976; Stackebrandt et al., 1997). A blast search has revealed that C.

All these results led us to the conclusion that Sch9 regulated localization of Bcy1 via Zds1. Bcy1 modification was found to be dependent on Yak1 (Griffioen et al., 2001). It was reported that faster-migrating iso-form of Bcy1-HA was detected in exponential phase wild-type cells, whereas a predominant slower-migrating iso-form of Bcy1-HA was

detected in stationary phase wild-type cells. But a predominant faster-migrating iso-form of Bcy1-HA was detected SCH772984 in yak1Δ mutant in either exponential phase or stationary phase. Recently, we reported that the faster-migrating iso-form of Bcy1-HA was detected in sch9Δ mutant cells, either in exponential phase or in stationary phase (Zhang et al., 2011). To investigate whether Sch9 regulated Bcy1 phosphorylation via Yak1, we tested whether Sch9 affected the protein level of Yak1. Figure 7a, shows that the protein level of Yak1 in log-phase glucose-grown sch9Δ cells (Line 2) was markedly lower than in log phase glucose-grown W303-1A (Line 1). The protein level of Yak1 in stationary phase W303-1A (Line 3) was dramatically lower than in the log-phase W303-1A (Line 1), whereas a predominant slower-migrating iso-form AZD6244 of Yak1-HA was detected in stationary phase sch9Δ (Line 4). As shown in Fig. 7b, the protein level of Yak1 in glycerol-grown sch9Δ cells was markedly lower than in glycerol-grown W303-1A (Line 1). Phosphatase treatment of this

slower-migrating iso-form of Yak1-HA resulted in the fast-migrating iso-form of Yak1-HA (Fig. 7b). These results suggest that Sch9 is involved in the regulation of Yak1 phosphorylation. In multicellular organisms, AKAPs targeted PKA holoenzyme to specific subcellular locations (Griffioen & Thevelein, 2002). AKAP-mediated targeting Tobramycin of PKA was thought to confer spatio-temporal control of PKA signaling to phosphorylate specific localized substrates. Compartmentalization of signal transduction pathways is an important spatio-temporal control of PKA signaling. In this way, signaling molecules of the same pathway are

brought into close vicinity, thereby increasing the probability that they only affect each other appropriately. Recently, we reported that Bcy1 was predominately localized in nucleus in sch9Δ cells, whereas a large part of catalytic subunits of PKA transferred from nucleus into cytoplasm in sch9Δ cells (Zhang et al., 2011). Thus the liberated catalytic subunits were not restricted by the regulatory subunits and consequently able to phosphorylate preferentially substrates located nearby (e.g. fructose-1,6-bisphosphatase, trehalase), all leading to a high PKA activity phenotype of sch9Δ cells. Our research indicated that Sch9 regulated localization of Bcy1 via Zds1. In yeast, Zds1 may act as the anchor protein of PKA. We report for the first time that Sch9 and Zds1 interact physically. However, the mechanisms of Sch9 regulating Zds1 still need to be clarified.

1a, plate 5), ConA ABT 199 reactivity of the Apa protein (Fig. 1b, lane 5 and c, lane 5), and in vitro labeling of polyprenyl phosphate (Fig. 2, lane 5). In mycobacteria and corynebacteria, Lnt and Ppm are either functional domains of the same protein (as in M. tuberculosis) or separate proteins encoded by contiguous genes that often exhibit translational coupling (Gurcha et al., 2002). All Streptomyces genomes sequenced to date reveal that the genes encoding Ppm are not preceded by those encoding homologues

of the Lnt domain of PpmMtu; instead, Streptomyces genomes show the presence of two genes encoding homologues of Lnt located separately on the chromosome. It has recently been shown in Streptomyces scabies that Lnt1, the homologue learn more exhibiting higher identity (44%) to Lnt of mycobacteria is functional, whereas the functionality of Lnt2, which exhibits only 26% identity, is still unclear (Widdick et al., 2011). We obtained a derivative of the wild-type J1928 with an in-frame deletion of the lnt1 gene (sco1014) and tested this strain (IB65, Table 1) for phage infection. Figure 3a (plate 3) and Table S2 show that φC31 was able to form plaques in the Δlnt1 mutant IB65; in addition, Apa protein obtained from this strain was recognized by ConA, indicating that it was glycosylated (data

not shown). Previous works have shown that the Lnt domain of PpmMtu is required for full Ppm activity and that it might anchor the catalytic domain (D2) to the membrane, in order to mannosylate the membrane polyprenyl phosphate (Gurcha et al., 2002). We therefore determined whether the PpmMtu D2 domain could complement the Δppm mutant in the absence MG-132 clinical trial of Lnt1. To do this, a double mutant was obtained with deletions of both the ppm and lnt1 genes (strain IB67, Table 1). Plasmids

expressing PpmSco (pBL13) or only the D2 domain of PpmMtu (pBL11) were introduced into the Δppm Δlnt1 mutant IB67 and analyzed for their ability to restore phage infection. Results shown in Fig. 3a and Table S2 reveal that, as expected, φC31 was unable to form plaques in IB67 (Fig. 3a, plate 4) and that plaque formation in the double mutant was restored by complementation with either PpmSco (Fig. 3a, plate 5) or the PpmMtu D2 domain (Fig. 3a, plate 6), meaning that Lnt1 is dispensable for Ppm activity in S. coelicolor. Given this observation and the difference in gene arrangement between streptomycetes and mycobacteria (Fig. S2), we asked whether the domain interaction previously reported between the D1 (Lnt) and D2 (Ppm) domains of PpmMtu (Baulard et al., 2003) was also shown by Lnt1 and PpmSco. To answer this, the S. coelicolor lnt1 and ppm genes were cloned in the bacterial two-hybrid system of Karimova et al.

Concerning immunity, although the mean CD4 cell count has increased significantly in the HAART era, it remains below average values found in the noninfected population. The association of candida oesophagitis with viral load has not been previously reported. The mechanism of this association is not clear, but could be linked to a reduction of PARP inhibitor review mucosal macrophage activity generated by the virus. Finally, factors related to HAART, such as viral resistance and nonadherence to therapy, could indirectly play a role in the relatively high prevalence of candida oesophagitis. In the HAART era, a reduced prevalence of Kaposi sarcoma was also

observed. This AIDS-defining cancer occurs at low CD4 cell counts. The decline in incidence during the HAART era confirms that immunosuppression is a key factor in the growth of this neoplasia in HIV-infected patients. The association between HAART and the incidence of Kaposi sarcoma has been shown by other groups [12,13]. A higher rate of both symptoms GSK126 manufacturer and endoscopic features of GERD was seen in our patients in the

HAART era. This has not been previously reported. The frequency of GERD in the early HAART period was close to that observed in the noninfected general population undergoing UGIe for reflux complaints, with GERD being found in approximately 30% of the patients [14]. This frequency continued to increase in the recent HAART period. We hypothesize that this increase could be explained by several factors. Firstly, the mean patient age in the recent HAART era Glycogen branching enzyme was higher than in the pre-HAART era, and was close to that of the general population [15]. Secondly, the improvement in the quality of life of HIV-positive patients might enable these patients to adopt behaviours that could favour gastroesophageal reflux, such as alcohol consumption, high-calorie food intake, tobacco addiction and weight gain [14]. We also found a significantly higher prevalence of HP infection in the HAART period, with a prevalence similar to that observed in the general population in Western countries (18–32%) [16,17]. Several hypotheses

to explain this can be proposed: higher acidic secretion in patients during the HAART period, contrasting with gastric hypoacidity seen in advanced stages of HIV infection in the pre-HAART era [18], associated with immune improvement (increased CD4 cell counts) allowing an effective inflammatory response could provide the favourable conditions needed for HP growth [19,20]. Alternatively, the use of chemoprophylaxis with agents against HP, such as macrolides, significantly decreased during the HAART era and this could also have contributed to the increase in the prevalence of HP infection. Whether gastric HP infection increases or decreases the frequency of GERD in the general population is still unclear [21]. Our results showed similar increases in the prevalences of both HP infection and GERD.

4c). These results provide strong evidence that the mechanism of action of sulphonamides and related

antifolate compounds is not connected with the salicylate metabolism as there was no change in the response of the PAS-hypersensitive mutants to these compounds. The evidence being presented in this paper is strongly supportive of our previous contention that PAS acts as an antimycobacterial agent by targeting the conversion of salicylate to mycobactin and carboxymycobactin (Ratledge & Brown, 1972; Brown & Ratledge, 1975). This is probably by the inhibition of salicylate http://www.selleckchem.com/products/Thiazovivin.html kinase (Adilakshmi et al., 2000), which converts salicylate via salicyloyl–AMP to salicyloyl–serine as part of the mycobactin/carboxymycobactin pathway (Ratledge, 2004). If Navitoclax PAS acted on another pathway, for example the PABA/folate pathway, then it would be very difficult to account for why the present knockout mutants of salicylate biosynthesis are

hypersensitive to PAS. There is an increase by over two orders of magnitude of the inhibitory effect of PAS in these mutants. In our view, the reason for this hypersensitivity is that salicylate synthesis is absent (or extremely low) in the knockout mutants and thus PAS can directly inhibit salicylate kinase without competition from the natural substrate, salicylate. Furthermore, the reversal of PAS inhibition in the mutants by salicylate, mycobactin and carboxymycobactin again strongly supports this hypothesis. Despite this and our previous advancement of this hypothesis, some arguments asserting that PAS is a metabolic analogue of PABA and interferes with the synthesis of folic acid continue to be advanced. Rengarajan et al. (2004) based their proposal

for PAS being Urease an antifolate inhibitor on evidence showing that when the thymidylate synthase (thyA) gene in Mycobacterium bovis was disrupted, this led to resistance towards PAS and also to known antifolate compounds. In addition, clinical isolates of M. tuberculosis that were resistant to PAS harboured mutations in thyA, but this was only in three out of eight isolates and therefore presumably the other five did not. A more recent study of Mathys et al. (2009) found that 63% of PAS-resistant clinical isolates of M. tuberculosis had no mutations in any of the nine genes they studied including six genes of the folate metabolic pathway. They did find, though, that specific mutations in the thyA gene were associated with increased PAS resistance and this then led them to suggest that PAS may, like other antimycobacterials (e.g. isoniazid and ethionamide), be a prodrug requiring activation by a functional ThyA enzyme, and thus when ThyA is inactive, PAS will not be converted to its active form. This view would then reconcile the views of Rengarajan et al. (2004) while still being in keeping with our own observations and conclusions regarding the action of PAS as a salicylate analogue.

The nucleotide variations in the gyrB sequences of the type strains of Stenotrophomonas spp. follow

the same pattern as that observed for the genes of the strains for which the genome sequences have been determined. The greatest variation was observed in the 3′ region of the gene, corresponding to gyrB Region 2 (Fig. 1). In the Stenotrophomonas genus, the gyrB Region 1, comprising 915 nucleotides, corresponds to 37% of the complete gene and included 306 variable nucleotide positions (33% of the sequence). The gyrB Region 2, comprising 705–711 nucleotides, corresponds to 29% of the gene and included 377 variable nucleotide positions (53% of the sequence). The amplified gyrB Regions 1 and 2 of the Stenotrophomonas strains investigated were of the same nucleotide lengths, respectively, with the exception of the gyrB Selleck Dasatinib Region 2 sequence of S. koreensis CCUG 53887T, which contained a gap of six nucleotides. The gyrB sequence similarity between the type strains of the 12 Stenotrophomonas spp. was as low as 82.0% for Region

1 and 71.1% for Region 2 (Fig. 2b, c and Table S2). The levels of sequence similarities, with few exceptions, were lower in the gyrB Region 2. The gyrB Region 1 and Region 2 of most of the Stenotrophomonas species type strains were < 92.8% and 92.3%, respectively, similar to that of the selleck chemicals llc type strains of any other species (Table S2). The exception to these findings were the type strains of S. maltophilia and S. pavanii, for which the sequence similarities of the two gyrB regions were 95.4% and 93.7%, respectively. The type strains of the S. acidaminiphila CCUG

46887T and S. nitritireducens CCUG 46888T exhibited gyrB Region 1 and Region 2 similarities of 92.8% and 92.3%, respectively. The genomic DNA similarity between the type strains of these two species (65.7%) and 99.4% 16S rRNA gene sequence similarity do indicate a close phylogenetic relationship between these species (Assih et al., 2002). S. daejeonensis gyrB Region 1 and Region 2 were 92.4% and 92.0% similar, respectively, to those of its closest relative, the S. acidaminiphila type strain. Protein kinase N1 Those two species exhibited 97.9% 16S rRNA gene sequence similarity and lower levels of genomic DNA similarity (34%) (Lee et al., 2011). For all other Stenotrophomonas spp., the sequences of both gyrB regions were < 91% similar to any other species. Also included in this study was the type strain of ‘Pseudomonas’ pictorum, CCUG 3368T, which has been shown previously to be closely related to Stenotrophomonas spp. (Van den Mooter & Swings, 1990; Anzai et al., 2000). Both gyrB regions of ‘P’. pictorum were observed to be < 90% similar to those of any Stenotrophomonas spp. type strain; this level of gyrB sequence difference is in same range as that observed between other Stenotrophomonas spp.

1/180.0 and an oxygenated sp2 carbon at δ 157.9, whereas a methoxy group at δ 4.00 coupled only with the latter carbon. The 13C NMR spectrum exhibited

additionally five quaternary and four sp2 methine carbons. Further HSQC and HMBC data (Fig. 3) suggested structure 1. Whereas the weak signal of C-8a showed the expected correlations with H-5 and H-7, the strongly broadened signal of C-9a could only be identified by comparison with authentic spectra: compound 1 is a new natural product but had been obtained previously by synthesis (Hagiwara et al., 2000; Knölker et al., 2002): the spectral data of the synthetic and natural 1 were identical within the error limits. Metabolites 2 and 3 were identified as carbazomycin D and F by spectroscopic analysis and comparison with the literature (Kondo et al., 1986; Naid et

al., 1987; Laatsch, 2011). Compound 1 ALK inhibitor drugs has been used as key intermediate in the synthesis of carbazomycins A, B, G (Knölker Afatinib cell line & Fröhner, 1997; Knölker & Schlechtingen, 1997; Hagiwara et al., 2000; Knölker et al., 2003), and carbazoquinocin C (Knölker et al., 2002) but this is the first report on its isolation from nature. It is plausible that compound 1 and the carbazomycins D (2) and F (3), which also had been isolated in this study, are in a biosynthetic relation. The nematicidal activity of the carbazole-1,4-quinones isolated here and further derivatives will be investigated in future experiments. This research was supported by The Royal Golden Jubilee PhD Program (PHD/0064/2549) and DAAD. The Graduate School of Chiang Mai University is also thankfully acknowledged. We thank Prof. Dr H.-J. Knölker (University of Dresden, Germany) for kindly providing NMR spectra of synthetic 1. Appendix S1. Mass, 1H NMR, 13C NMR, HMBC and HSQC Protirelin spectra of 3-methoxy-2-methyl-carbazole-1,4-quinone; Mass and 1H NMR spectra of carbazomycin D and,

Mass and 1H NMR spectra of carbazomycin F. 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. “
“Two bacterial strains (DY05T and 47666-1) were isolated in Queensland, Australia, from diseased cultured crustaceans Panulirus ornatus and Penaeus monodon, respectively. On the basis of 16S rRNA gene sequence identity, the strains were shown to belong to the Harveyi clade of the genus Vibrio. Multilocus sequence analysis using five housekeeping genes (rpoA, pyrH, topA, ftsZ and mreB) showed that the strains form a monophyletic group with 94.4% concatenated sequence identity to the closest species. DNA–DNA hybridization experiments showed that strains DY05T and 47666-1 had 76% DNA similarity to each other, but <70% to their closest neighbours Vibrio harveyi LMG 4044T (≤55%), Vibrio campbellii LMG 11216T (≤52%) and Vibrio rotiferianus LMG 21460T (≤46%).