Type IV pili also function in bacterial conjugation (Proft & Baker, 2009), an active mechanism within biofilm cells, being responsible for the transference

of genetic material including genes of resistance against antibiotics (Molin & Tolker-Nielsen, 2003). Interestingly, the treatment of X. fastidiosa with gomesin upregulated the expression of plasmid genes, including one gene encoding a conjugal transfer protein (traG or virB11). Besides involvement in adhesion to substrata and cell-to-cell aggregation, STAT inhibitor bacterial biofilms are also involved in bacterial resistance to many antimicrobial agents (Mah & O’Toole, 2001). In addition to the upregulation of CDS related to biofilms, the treatment of X. fastidiosa with a sublethal concentration of gomesin indeed leads to an enhancement in biofilm production. This does not seem to be a general effect to all antimicrobial agents, because exposure of X. fastidiosa to a sublethal concentration of streptomycin showed no effects on biofilm production. It has been reported that bacteria treated with sublethal concentrations of antimicrobial agents can increase or diminish biofilm production (Drenkard & Ausubel, 2002; Overhage et al., 2008; Jones et al., 2009). In Neisseria meningitidis, a sublethal concentration of

LL-37, a human cathelicidin, induces the formation of the a polysaccharide capsule (Jones et al., 2009). Conversely, this same AMP was reported to inhibit the biofilm production by Pseudomonas aeruginosa (Overhage et al., 2008). On the other hand, conventional MG-132 mouse antibiotics were reported to stimulate biofilm production by this same bacterium (Drenkard & Ausubel, 2002). These

results clearly demonstrate that the response of bacteria to a sublethal concentration of antimicrobial agents depends not only on the bacterial strain but also on the nature of the drug. When X. fastidiosa pre-exposed to 50 μM of gomesin was inoculated into tobacco plants, Mannose-binding protein-associated serine protease fewer plants displayed foliar lesions relative to control plants (inoculated with nontreated bacteria) 30 days after inoculation (Fig. 3). This result suggests that due to the enhancement in biofilm production, bacteria may be trapped to fewer vessels of the plant xylem, causing a delay in the appearance of symptoms. Indeed, the above-described mutants of the X. fastidiosa Temecula strain defective for the production of the hemagglutinin HxfA, despite having a reduced ability to adhere to a glass surface and also to form cell-to-cell aggregates, were surprisingly hypervirulent to grapevine, due to an increased number of infected vessels of the plant xylem (Guilhabert & Kirkpatrick, 2005). On the other hand, limiting bacteria to a few vessels of the plant could have the opposite effect, diminishing disease symptoms. Together, our results demonstrate that gomesin modulates the global gene expression of X. fastidiosa at a sublethal concentration, inducing genes involved in biofilm production, among others. Indeed, X.

3b), (3) wrinkled cells (Figs 3c and 4a–c), and (4) the formation of cell clusters (Fig. 4a). Quantitative analyses revealed that membrane disruption and wrinkled cells were the most common alterations observed (Fig. 5). A small increase of rounded cells (Figs 3d and 4a–c) percentage was observed in T. vaginalis treated with AZA whereas fewer of these cells were found after EIL treatment (Fig. 5). However, no change was observed on endoflagellar forms (pseudocysts). These cells appear under unfavourable environmental conditions when the flagella are internalized, and a true cell wall is not formed (Pereira-Neves et al., 2003). In addition, changes LBH589 in intracellular structures

were also observed. Several important alterations were observed at the ultrastructural level in the drug-treated trophozoites, including (1) Golgi duplication, (2) vesicles containing membranous Luminespib supplier profiles (Fig. 4d), (Fig. 6a–c), (3) altered and enlarged Golgi cisternae (Fig. 4e, arrow) and (4) abnormal hydrogenosomes, which are seen as electron-lucent organelles (Fig. 4d–f). Autophagy was also detected, as evidenced by the membranous profiles of endoplasmic reticulum that were surrounding the hydrogenosomes (Fig. 4f,

arrowhead). Giardia lamblia treated with AZA and EIL also presented similar results (Maia et al., 2007) and this autophagic process suggests that the cells were implementing a survival strategy under stress conditions (Edinger & Thompson, 2004). Many of these alterations have previously been shown in T. vaginalis treated with hydrogen peroxide (Mariante et al., 2003), taxol (Madeiro

da Costa & Benchimol, 2004), nocodazole (Madeiro da Costa & Benchimol, 2004) or griseofulvin (Mariante et al., 2006). It is important to note that the phenomena described above, such as membrane blebbing, vacuolization and autophagy, are features typical of cell death, and they have been described previously in trichomonads (Mariante et al., 2006; Benchimol, 2008). Moreover, the presence of autophagic vacuoles may be indicative of membrane recycling, thus aiding in the remodelling of the cell (Maia et al., 2007). However, in previous studies of T. vaginalis treated with metronidazole, the main alteration observed was a reduction in hydrogenosomes’ Amine dehydrogenase size (Land et al., 2001; Wright et al., 2010). On the other hand, in mammalian cells (MDCK cells) where the enzyme target is also absent, no morphology alteration was observed by SEM and TEM (Supporting Information, Figs S1 and S2). Mammalian cells, such as MDCK and Caco cells, did not exhibit any apparent damage when treated with 5 μM AZA or 10 μM EIL for 24 h and analysed using the MTT viability test (Fig. S3). This is a very important observation, as it suggests that the experimental compounds have selective antiparasitic effects. Taken together, the results suggest that azasterols could be important compounds in the development of novel chemotherapeutic approaches against T. vaginalis.

Until data are available, this preparation is not advised for this group. In the pre-HAART era, HIV-infected children responded poorly to HBV vaccine [73]. Post-HAART, a study evaluating the response to revaccination after immune recovery on antiretroviral therapy (ART) demonstrated that those with complete virological suppression at the time of revaccination achieved protective vaccine responses [74], however protective

responses were achieved less frequently in children under 2 years of age [75]. It is not currently known whether larger doses of vaccine, as are used for other groups with underlying disease, are more effective for HIV-infected children; some clinicians advocate using adult doses of vaccine to immunize HIV-infected children [76]. Periodic measurement of HBV antibody status is also recommended, especially if there is likely to be a risk of ongoing exposure [77]. HAV vaccine has a good safety profile, supporting its LDE225 mw use in HIV-positive children, especially those with liver disease or HBV or hepatitis C virus (HCV) coinfection [78]. A study of the standard two-dose schedule given 1 month apart showed low antibody titres and limited persistence in 235 HIV-infected children on effective HAART; a third dose was found to be safe and resulted in increased antibody titres [79]. Another study demonstrated that all HIV-infected children, including those with HBV

coinfection, Proteasome inhibitor drugs had adequate responses after two doses of HAV vaccine if given more than 6 months apart [80]. Combined HAV and HBV vaccines are advantageous for HIV-infected children as they minimize the number of injections received. As for HBV, the adult preparation may be preferable but this strategy is not yet evidenced. Annually revised seasonal influenza vaccines contain killed viruses and so are safe for HIV-infected

children over 6 months of age; two doses are given in the first year of receiving the vaccine, and then a single dose is given annually thereafter, ideally before the influenza season begins. Evidence on efficacy in HIV-positive children on HAART is limited. A study comparing influenza vaccine responses in healthy versus HIV-infected children showed poor antibody responses in the latter, despite effective HAART [81]. Thus, in addition Clomifene to vaccinating all HIV-positive individuals against seasonal flu annually, also vaccinating household contacts reduces exposure to influenza in the family setting. At the time of writing, seasonal influenza vaccines appear to confer little or no cross-reactive antibody responses to 2009 H1N1 [82], so vaccination against pandemic influenza strain A/H1N1 is currently recommended for all HIV-infected patients. A recent study using an MF59-adjuvanted H1N1 influenza vaccine demonstrated that it was immunogenic, safe and well tolerated in HIV-infected children and adolescents [83].

, 2009). For Cry3A protein (the most important coleopteran-specific Cry toxin), loop 1 has an important function in biological activity: the mutations ABT-263 order R345A, Y350F, Y351F, ΔY350 and ΔY351 showed higher levels of toxicity against Tenebrio molitor (Coleoptera) (Pardo-López et al., 2009). SN1917 has several changes related to these observations, with respect to the parental Cry1Ba (R345Q, Y349M and ΔY350). It may be that these residues are important factors of activity, for example arginine has a positive

charge because the guanido group is ionized over the entire pH range in which proteins exist naturally, and the hydroxyl group of the phenolic ring of tyrosine residues makes this aromatic ring relatively reactive in electrophilic substitution reactions (Creighton, 1993). On the other hand, anticoleopteran Cry proteins are only toxic after in vitro solubilization, probably because the protoxin cannot be solubilized at the neutral to weakly acidic gut pH of Coleoptera (de Maagd et al., 2001). For the midgut and the hindgut of CBB, values between pH 4.5

and 5.2 were consistently observed (Valencia et al., 2000). This result suggests that there is an important activity determinant in check details domain II of Cry1Ba, although it may be a nonspecific binding. For this reason, further study of CBB physiological conditions and mutagenesis Edoxaban site-directed in this toxin and other related Cry proteins is necessary.

The authors are grateful to Dr Ruud A. de Maagd for his participation to this project and the critical discussion of this paper. This work was supported by Dirección de Investigación de la Universidad Nacional de Colombia sede Bogotá (Colombia). S.A.L.-P. gratefully acknowledges Colciencias for his PhD fellowship. “
“The SbmA protein is involved in the transport of MccB17-, MccJ25-, bleomycin- and proline-rich peptides into the Escherichia coli cytoplasm. sbmA gene homologues were found in a variety of bacteria. However, the physiological role of this protein still remains unknown. Previously, we found that a combination of sbmA and tolC mutations in Tn10-carrying E. coli K-12 strains results in hypersusceptibility to tetracycline. In this work, we studied sbmA expression in a tolC mutant background and observed an increased expression throughout growth. We ruled out the global transcriptional regulator RpoS and the small RNA micF as intermediates in this regulation. The tolC mutation induced the expression of other well-characterized strong σE-dependent promoters in E. coli.

, 2007). For example, in Fig. 1A, the delay R1 was ∼40 ms and the Gaussian curve peaked at ∼60 ms, thus ∼100 ms after the previous motor unit discharge, i.e. a discharge rate of ∼10 Hz (Bawa & Lemon, 1993). The delay R1 was adjusted according to the

motor unit firing rate, so that TMS was delivered within the recovery phase of the after-hyperpolarization. Thus, when the computer triggered a single TMS pulse at check details delay R1, the effects on the membrane potential of the motoneuron are optimized, and peak(s) appeared in the PSTH (from an FDI unit) 20–35 ms after TMS (Fig. 1B). The(se) peak(s) reflect(s) the arrival of corticospinal input(s) at motoneuron level, and indicate(s) that the resulting corticospinal excitatory post-synaptic potential(s) [EPSP(s)] were sufficient to advance the find more discharge of the motoneuron, as compared with its firing rate during voluntary contraction, by shortening the after-hyperpolarisation duration (Fig. 1A and B). The peak in the PSTH is correlated to the ascending phase of the underlying EPSP at motoneuron level (Kirkwood & Sears, 1978; Ashby &

Zilm, 1982). Therefore, the TMS-induced peak in PSTH can be used to estimate the corticospinal EPSP produced at the motoneuron level. The hot spot for FDI and the RMT were determined at the beginning of the experiment. The intensity of both test and conditioning pulses influences the level of SICI (Chen et al., 1998; Sanger et al., 2001; Orth et al., 2003; Roshan et al., 2003; Garry & Thomson, 2009; Lackmy & Marchand-Pauvert, 2010). Therefore, the test pulse intensity was changed so as to evoke a peak in the PSTH of different size (normalized to the number of stimuli, see PSTH analysis below), reflecting corticospinal EPSPs of different size. It was necessary to adjust the intensity of the conditioning pulse to produce SICI without evoking a peak in the PSTH, to prevent possible Diflunisal summation of corticospinal volleys (induced by the test and conditioning pulses) at the motoneuron level. As a consequence, the conditioning pulse could only be set to 0.6 RMT, an intensity at which TMS did not

produce a peak in the PSTH (Fig. 1C) but was sufficient to activate SICI (Fisher et al., 2002). At 0.65 RMT, a peak occurred in the PSTH of some motor units (see Results). A recording session consisted of sequential alternation (0.3 Hz) of isolated test and paired pulses (conditioning + test pulses with a 2-ms interval), to deliver as many test pulses (test peak) as paired pulses (conditioned peak). To avoid muscular fatigue (which can develop rapidly in FDI), 30–50 single and 30–50 paired pulses were delivered during each recording session; the session was stopped when the subjects developed fatigue or had difficulty in maintaining a steady motor unit discharge. Care was taken to ensure that the same motor unit was studied in each session, based on the shape of the potential, its firing rate, the hand position and the movement performed by the subject, and the peak latency in the PSTH.

8% at months 12, 24, 36 and 48, respectively). Regarding plasma lipid levels (Fig. 1d and e) we did not observe significant changes during the follow-up period. We found hypercholesterolaemia (>200 mg/dL) in 9.5, 30.4, 21.7, beta-catenin inhibitor 14.3 and 13.3% of patients at months 0, 12, 24, 36 and 48, respectively, and hypertriglyceridaemia (>170 mg/dL) in 14.3, 8.3, 13, 4.5 and 0% of patients at the same time-points. Throughout follow-up, and especially at the end of the study, we found an increase in plasma resistin and significant increases in total plasminogen activator inhibitor type 1 (tPAI-1), adiponectin and leptin levels (P<0.05) (Fig.

1f–i). Regarding the leptin:adiponectin ratio, HOMA values and C-peptide levels, we observed a slight increase during the first few months on HAART followed by a moderate decrease or stabilization after 24 months on HAART (Fig. 1j–l). The median BMI did not change significantly during follow-up, with values being between 17.32 and 16.42. There were no children in the overweight and low-weight BMI categories. Dasatinib molecular weight Concerning diagnoses of lipoatrophy, 17 children had no lipoatrophy, three had mild lipoatrophy, five had moderate lipoatrophy and two had severe lipoatrophy. Overall, seven of the 27 patients (25.9%) had lipoatrophy with scores ≥2. Concerning lipohypertrophy, 16 children did not have lipohypertrophy, three had mild lipohypertrophy, five had moderate lipohypertrophy and three had severe

lipohypertrophy. Overall, eight of the 27 patients (29.6%) had lipohypertrophy with scores ≥2. By the end of the study, 12 of the 27 children (44.4%) had lipodystrophy. However, only three of the 27 children (11.1%) had both lipoatrophy and lipohypertrophy scores ≥2. We carried out a follow-up study in PI-naïve HIV-infected Dichloromethane dehalogenase children on HAART for 4 years, and found an increase in adipokine levels. This increase could be related to the

direct effect of PIs on adipose tissue, which could contribute to an imbalance in lipid metabolism and spatial development of lipodystrophy and metabolic syndrome in HIV-infected patients [21]. The metabolic pathway and the cytokine profile accomplices in the development of lipodystrophy and lipoatrophy is very complex. Thus, we did not find any significant trend in adipokine kinetics that may be associated with the onset of lipodystrophy at the end of the study. Moreover, results did not differ between patients with complete HIV suppression and those failing therapy. Therefore, we cannot definitely conclude from these results that there is a direct effect of HAART on adipose tissue, but there is a trend that warrants further investigation in studies with another design. In the present study we used clinical assessments of lipodystrophy; Dual Energy X-ray Absortiometry (DEXA) scanning would have provided a more quantitative assessment of lean vs. fat mass (particularly visceral fat) and may have provided better insights into the potential relationship between fat changes and adipokine levels.

Transplantation 2008; 85: 359–368. 28  Duclos-Vallee JC, Feray C, Sebhag M et al. Survival and recurrence of hepatitis C after liver transplantation in patients co-infected with human immunodeficiency virus and hepatitis C. Hepatology 2008; 47: 407–417. 29  Terrault N, Roland ME, Schiano T et al. Outcomes of liver transplant recipients with hepatitis Y-27632 supplier C and human immunodeficiency virus coinfection. Liver Transpl 2012; 18: 716–726. 30  Miro JM, Montejo M, Castells L et al. Outcome of HCV/HIV-coinfected liver transplant

recipients: a prospective and multicentre cohort study. Am J Transplant 2012; 12: 1866–1876. 31  Cooper C, Kanters S, Klein M et al. Liver transplant outcomes in HIV-infected patients: a systematic review and meta-analysis with synthetic cohort. AIDS 2011; 25: 777–786. 32  Coffin CS, Stock PG, Dove LM et al. Virologic and clinical outcomes of hepatitis B virus infection in HIV-HBV coinfected transplant recipients. Am J Transplant 2010; 10: 1268–1275. 33  Antonini TM, Sebagh M, Roque-Afonso AM et al. Fibrosing cholestatic hepatitis in HIV/HCV co-infected transplant patients – usefulness of early markers after liver transplantation. Am J Transplant 2011; 11: 1686–1695. 34  Joshi D, O’Grady J, Taylor C, Heaton N, Agarwal K. Liver transplantation in human immunodeficiency virus-positive patients. Liver Transpl 2011; 17: 881–890. The Writing Group

thanks the BHIVA Secretariat for administrative help, Alison www.selleckchem.com/products/c646.html Richards for conducting the systematic literature search and Jacoby Patterson for work on critical appraisal, evidence profiles and construction of GRADE tables. The Writing

Group also thanks Dr Ashley Brown, in his role as Chair of the British Viral Hepatitis Group (BVHG), for his valuable advice and input; Dr Hilary Curtis, for advising and overseeing the development of the Auditable Outcomes; and Dr Adrian Palfreeman and Prof Martin Astemizole Fisher for regulating and advising on the development of the guideline according to the process laid down by the National Institute for Health and Clinical Excellence (NICE). The Writing group also thanks Dr Gail Matthews and Dr Curtis Cooper for their peer review of the guidelines. Dr Ed Wilkins has received advisory board honoraria, speaker fees, and travel/registration reimbursement from Gilead, Merck Sharp and Dohme, Bristol-Myers Squibb, Abbott, Janssen, Boehringer Ingelheim and ViiV. Dr Mark Nelson has received fees from Gilead, Merck Sharp and Dohme, Bristol-Myers Squibb, Abbott, Janssen and ViiV. He has received research funding from Gilead, Merck Sharp and Dohme, ViiV, Janssen, Boehringer Ingelheim and Bristol-Myers Squibb. Dr Kosh Agarwal has received lecture honoraria, speaker fees, and travel/registration reimbursement from Gilead, Merck Sharp and Dohme, Bristol-Myers Squibb, Janssen and Boehringer Ingelheim, and research grants from Roche and Gilead. Ms Dola Awoyemi has no conflicts of interest to declare.

Within the various subclusters, further discrimination reflected the polymorphism revealed by restriction analysis of the tested loci (Table 3). GapC gene resulted the most conserved among the tested strains; in fact, restriction analysis of the amplified fragment with different restriction enzymes did not reveal sequence variations among the strains, with

the exception of isolate V79 from fish, which differentiated from the other strains when HaeIII was employed (Identification profile in Table 3 = Ip 24). Restriction analysis of the galP amplicon grouped the strains into two main clusters, within which the distribution of strains was always the same, even using different enzymes. One cluster (named ‘meat-group’, Ip 1, 4, 9, and 12) contained all meat isolates (with the exception of Sa113), two salad isolates and eight of the 12 fish isolates; the second cluster (named ‘dairy-group’, JAK drugs Ip 3, 5, 8, and 10) included all dairy isolates and the remaining vegetables and fish isolates. The isolate

from wheat flour always grouped with strains of dairy origin. Strain Sa113 from meat products showed a unique restriction profile (Ip 2, 6, 7, and 11). Restriction analysis of the atpA gene with RsaI delineated Fulvestrant ic50 the same two clusters obtained when galP gene was tested; in this case, Sa113 grouped whit meat isolates (Ip 16). Also using HpaII, the differentiation among strains was respected (meat-group, Ip14 – dairy-group, Ip 15) with an additional discrimination for four meat isolates (Smp1-2-3-4, Ip 13). The digestion of tuf gene with RsaI grouped two meat isolates (Po1 and Tac2) with dairy-group (Ip 19), while the use of HhaI permitted the separation of Sa113 (Ip 20) and the differentiation of dairy isolates and Po1 and Tac2 (Ip 22) from the remaining meat, fish and vegetable isolates (Ip 21). Restriction analysis isothipendyl of the dltA and als genes revealed further

polymorphisms, and the possibility to discriminate the two salad (Ip 28) and the cereal isolates (Ip 42) from the other strains and to highlight two sub-groups within dairy isolates (Ip 32, 33). PCR-ribotyping generated by digestion of total DNA with PstI, revealed the presence of nine different electrophoretic profiles, characterized by two to five bands of molecular weight varying from 4000 to more than 10 000 bp (Fig. 3). The data obtained indicate an important heterogeneity both in the copy number and in the distribution of the ribosomal operons along the chromosomal DNA, as evidenced in the corresponding dendrogram (Fig. 3). Two main groups were distinguished, at a low similarity level (0.36). The distribution of the tested strains within the main groups differed in part from that previously observed.

2,10 This creates a problem for the treating physician if relying on serological evidence of cure. A persistently elevated antibody titer following treatment may be interpreted as evidence of unresolved infection and consequently result in multiple treatment courses which may be unnecessary and associated with side-effects and additional cost.

We undertook a longitudinal prospective study of schistosomiasis serology in both travelers and immigrants in a nonendemic country to determine the natural history of schistosomiasis antibody titer post-recommended treatment in those who have not been reexposed. All adult patients presenting to the Victorian Infectious Diseases Service (VIDS) at the Royal Melbourne Hospital, Australia between July 1995 and December 2005 identified with

a positive GDC-0980 serological test for schistosomiasis (defined as titer greater than 1:64), and had received treatment for schistosomiasis without possible reexposure were considered for this study. Schistosomiasis serology was performed at baseline and at subsequent visits and grouped according to those performed within 3, 6, 12, 18, 24, and 30 months of treatment. Serology was identified as being greater than or equal to fourfold increase or decrease, twofold increase or decrease, conversion to negative or unchanged from baseline prior to treatment. All serological testing for schistosomiasis was performed by

the Victorian Infectious Diseases Reference Laboratory SB-3CT (VIDRL) in Victoria, selleck compound Australia using an IHA assay (Cellognost*-Schistosomiasis H, Behring, Germany). This test specifically detects total circulating antibodies to antigens of adult Schistosoma mansoni worms; however, due to the similarity of antigens, antibodies to Schistosoma haematobium and Schistosoma japonicum can also be detected. Although prepared with adult S mansoni worms, IHA has a 92% sensitivity and 94% specificity for detecting S haematobium.8 Cross-reactivity with other helminths has been reported due to shared antigenic determinants.11 These other helminthic infections were excluded where epidemiologically appropriate through relevant serology and fecal testing. Parallel testing of paired sera of individual patients was performed in > 90% of cases. The recommended treatment given to all patients in this study was praziquantel at a dose of 20 mg/kg twice daily for 3 days.12,13 At review, patients were assessed for adherence, evidence of persisting infection (symptoms, parasite detection on microscopy, or eosinophilia), and history of reexposure to endemic areas. Patients were excluded from the longitudinal study if serological testing was performed at an outside laboratory, if there was evidence of persisting infection, if there was a history of reexposure or if treatment was incomplete.

, 2009). We also found evidence of genetic exchange between Xanthomonas and Betaproteobacteria. A contig from Xcm 4381 (Fig. 2c) most

closely resembled the genome of Acidovorax species JS42 (95% sequence identity over 7935 nucleotides) and, slightly more distantly (94% identity over 3327 nucleotides), resembled the genome of X. campestris pathovar vesicatoria 85-10. This region encodes a predicted Small molecule library TrbK-like protein. TrbK is usually plasmid associated (Haase et al., 1996), but the corresponding genomic regions in Acidovorax species JS42 and in X. campestris pathovar vesicatoria 85-10 appear to be chromosomally located. It is unclear whether the 23-kb Xcm 4381 contig (Fig. 2c) represents a plasmid or is part of the chromosome. Plant-pathogenic Xanthomonas pathovars require a T3SS to secrete and translocate effector proteins (Alfano & Collmer, 2004; Yang et al., 2005; Grant et al., 2006; Gurlebeck et al., 2006;

White et al., 2006, 2009; Kay & Bonas, 2009; Buttner & Bonas, 2010) in order to cause disease. These effectors have evolved to manipulate host cellular processes to the benefit of the pathogen; however, many plants have evolved resistance whereby they can recognize specific effectors, triggering the hypersensitive response. Therefore, in the context of a resistant plant, these effectors show an ‘avirulence’ activity, thus limiting the pathogen’s host range (Alfano & Collmer, 2004; Yang et al., 2005; Grant et al., 2006; Gurlebeck et al., 2006; White et al., 2006, 2009; Glutathione peroxidase Kay & Bonas, 2009; Buttner & Doxorubicin in vitro Bonas, 2010). A single Xanthomonas genome

typically encodes 20–30 T3SS effectors. The repertoire of effectors varies between species and strains within species and is believed to be a key determinant in the host range of a given pathogen. The draft genomes of both Xcm 4381 and Xvv 702 encoded a complete T3SS apparatus. To identify homologues of known T3SS effectors, we used blast searches against catalogues of proteins from the Pseudomonas syringae Hop Identification and Nomenclature Home Page (http://www.pseudomonas-syringae.org/), The Xanthomonas Resource (http://www.xanthomonas.org/t3e.html) and papers by White et al. (2009) and Gurlebeck et al. (2006). In common with all previously sequenced Xanthomonas genomes, both draft genomes encode homologues of the candidate T3SS effectors AvrBs2, AvrGf1, XopF, XopK, XopL, XopN, XopP, XopQ, XopR, XopX and XopZ. Both strains also encode homologues of XopA, XopB, XopG, XopH, XopI, XopY, XopAA, XopAD, XopAE and XopAK, which are conserved in a subset of the previously sequenced Xanthomonas genomes (http://www.xanthomonas.org/t3e.html). Both Xcm 4381 and Xvv 702 also encode proteins sharing 71% amino acid sequence identity with P. syringae effector HopW1; these have no significant sequence similarity to any known Xanthomonas protein (Fig. 3). Both draft genomes contained genes encoding homologues of the P.