For each round of SCOTS, 3 μg cDNA

samples were denatured at 98 °C for 3 min and normalized by self-hybridization, and hybridized subsequently Sirolimus in vitro at 65 °C for 24 h with 0.6 μg photobiotinylated C51-17 genomic DNA that had been blocked previously with 5 μg 16S and 23S rRNA genes. The cDNAs were captured by streptavidin-coupled magnetic beads (Dynal M280, Invitrogen) according the manufacturer’s instructions. After elution, the cDNAs were re-amplified by PCR using the primer, SCOTS-01 or SCOTS-02. For each growth condition, in the first round of normalization, 10 separate samples of the cDNA mixture were captured by hybridization in parallel reactions and the 10 amplified cDNA preparations were combined for further procedures. To identify cDNA molecules that represented transcripts from genes that were specific to or upregulated in expression during growth of P. multocida in the liver, an enrichment process was included in the experiments as described previously (Hou et al., 2002). The final captured cDNAs were cloned into the pMD18-T vector (TaKaRa), and

the white clones on the X-gal plates were subjected to a Southern dot blot and sequenced using the standard Selleck BYL719 Sanger method. Database searches and DNA and protein similarity comparisons were carried out using the blast algorithm from the National Center for Biotechnology Information at the National Library of Medicine (http://www.ncbi.nlm.nih.gov/BLAST/Blast.cgi). Five microliters of PCR product from each clone was denatured by boiling and transferred onto a positively charged nylon membrane (Millipore, Billerica, Morocco). The cDNA mixture was amplified from three rounds of normalization using the specific primer SCOTS-01 or SCOTS-02 and labeled with digoxigenin (DIG)-labeling mix to form probes. Membranes were fixed, prehybridized and hybridized at 42 °C, and hybridization signals were detected using the DIG Detection Kit (Roche, Germany) according to

the manufacturer’s instructions. Total RNAs isolated from bacterial pellets and infected heptaminol livers were reverse transcribed as the same primers used earlier. The real-time PCR assay was performed using SYBR-Green dye (TaKaRa). Specific gene primers were designed for the qRT-PCR, and the sequences are shown in Table 1. Each 20 μL reaction included 100 ng cDNA, 200 nmol of each primer and 10 μL 2× SYBR-Green dye. The following cycles were performed: 95 °C for 3 min for the hot-start, followed by 40 cycles of 95 °C for 15 s, 65 °C for 30 s, and 72 °C for 45 s. The Ct value for the 40 cycles was recorded, and qRT-PCR analysis of P. multocida RNA derived from in vivo and in vitro cultures was performed for the test genes and the internal control of the 16S rRNA gene in triplicate. The relative level of expression was calculated using the method.

In both areas, these correlations were stronger in neurons showing delay selectivity than in those without delay selectivity. Notably, delay-selective neurons in A35 responded similarly to the optimal stimulus and its paired associate, whereas delay-selective learn more neurons in A36 discriminated between them. However, these neurons in both areas discriminated the primary pair, consisting of the optimal stimulus and its paired associate, from other pairs, indicating that selectivity across pairs was maintained between the two areas. These results suggest that delay-selective neurons in A35 represent these paired stimuli as a single unitized item rather than two associated items. “
“The

activity of neurons in the rostral ventrolateral medulla (RVLM) is critical for the generation of vasomotor sympathetic tone. Multiple pre-sympathetic pathways converge on spinally projecting

RVLM neurons, but the origin and circumstances in which such inputs are active are poorly understood. We have previously shown that input from the contralateral brainstem contributes to the baseline activity of this population: in the current study we investigate the distribution, phenotype and functional properties of RVLM neurons with commissural projections in the rat. We firstly used retrograde transport of fluorescent microspheres to identify neurons that project to the contralateral RVLM. Labelled neurons were prominent in a longitudinal column that extended over 1 mm caudal from the facial nucleus and contained hybridisation products indicating enkephalin STI571 manufacturer (27%), GABA (15%) and adrenaline (3%) synthesis and

included 6% of bulbospinal neurons identified by transport of cholera toxin B. Anterograde transport of fluorescent dextran-conjugate from the contralateral RVLM revealed extensive inputs throughout the RVLM that frequently terminated in close triclocarban apposition with catecholaminergic and bulbospinal neurons. In urethane-anaesthetised rats we verified that 28/37 neurons antidromically activated by electrical stimulation of the contralateral pressor region were spontaneously active, of which 13 had activity locked to central respiratory drive and 15 displayed ongoing tonic discharge. In six tonically active neurons sympathoexcitatory roles were indicated by spike-triggered averages of splanchnic sympathetic nerve activity. We conclude that neurons in the RVLM project to the contralateral brainstem, form synapses with sympathetic premotor neurons, and have functional properties consistent with sympthoexcitatory function. “
“Gamma protocadherins (Pcdh-γs) resemble classical cadherins and have the potential to engage in cell–cell interactions with homophilic properties. Emerging evidence suggests non-conventional roles for some protocadherins in neural development. We sought to determine whether Pcdh-γ trafficking in neurons is consistent with an intracellular role for these molecules.

These responses were initially predicted by clustering analysis, as these mutants fall into clusters being predicted involvements in blue light signalling (clusters I, II, IV and V) and those predictions involving blue, red and far-red light signalling (clusters III). These putative components of light signalling in Xcc included three HKs, four GGDEF-characterized

proteins and Osimertinib datasheet four hybrid HKs. Motility is an important characteristic for infection in a number of plant pathogenic species (Swings et al., 1993); thus, we tested whether PAS proteins participate in the development of motility in the Xcc in response to variable light conditions. Five of 33 mutants showed significantly modified motility responses to light (Fig. 3). Among them, DLT4313 was increased, and DLT0728, DLT0818 and DLT1965 were decreased in blue light. DLT1036 exhibited decreased motility in blue, red, far-red or white light. These results partially agreed with the results of clustering analysis (Fig. 1c), in which the protein altered in DLT0728 was associated with cluster IV and was a putative blue light–signalling component. learn more We cultured cabbage infected with Xcc strains under two levels of light intensity. The light intensity reaching into

a leaf was initially estimated in a light transmission assay, which indicated that a light intensity of 4512 and 593 lux reached the middle of a leaf exposed to light sources of 12 000 and 2000 lux, respectively (Fig. S2). The results of Xcc strains are shown in Fig. S3. We also tested rescue strains of three mutants, DLT1036, DLT 2324 and DLT3829. In assays of Xcc strains infecting cabbage, four mutants (DLT3829, DLT1036, DLT2324 and DLT1476) had an effect on light-condition-dependent shifts in bacterial virulence. Leaf-lesion photographs of the four mutants are shown in Fig. 4a (strong light) and 4b (weak light), and the mutants showed different changes in lesion length

(LL) in strong/weak light or between the two light intensities, as shown in Fig. 4c. The relative lesion rate (RLR) values of the four mutants were significantly different from check details wild-type Xcc 8004 (Fig. 4d). The tests of complementary strains are shown in Fig. S4, in which the virulence of pLC1036, pLC2324 and pLC3829 were partially rescued in comparison with either LL or RLR. In addition, three of the four mutants have been shown to be GGDEF-characterized proteins involved in virulence under natural light (Ryan et al., 2007). These data strongly suggest that these PAS proteins are light-signalling components that are vital for Xcc pathogenesis. Some of the PAS proteins in Xcc may have roles as intermediates in photo-signalling pathways other than light sensing, and some of those involved in light signalling may not have phenotypes that could be observed in our screen. Previous studies have suggested that PAS domains sense light, and the subsequent functions result in various responses, for example, a PAS domain can be activated in blue light to regulate B.

Some functional genes have been disrupted through the insertion of ISs, preferentially IS231C. By comparing the Southern hybridization profiles of different B. thuringiensis strains, the existence of ISBth166 was mainly found in serovar kurstaki and the recent expansion of IS231C between different kurstaki isolates was suggested. In addition to revealing the ISs profile in YBT-1520 as well as the comparison in the B. cereus group, this study will contribute to further comparative

analyses of multiple B. thuringiensis strains aimed at understanding the IS-mediated genomic rearrangements among them. The Bacillus cereus group consists of a group of gram-positive endospore-forming bacteria belonging to the Firmicutes phylum. Tofacitinib cost These species have a huge impact on human activities due to their pathogenic properties and/or economic importance, such as Bacillus anthracis, the causal agent of anthrax, which can be lethal to humans and other mammals; B. cereus, an opportunistic human pathogen involved in food-poisoning incidents and contaminations in hospitals (Drobniewski,

1993); and Bacillus thuringiensis, an insect pathogen that is widely used as a leading biorational pesticide (Schnepf et al., 1998). These three species are very closely related at the genomic level and were strongly suggested to represent one species on the basis of genetic evidence (Rasko et al., 2005; Tourasse et al., 2006). The only established difference between B. cereus and B. thuringiensis strains is the presence of genes coding for the insecticidal toxins, usually Palbociclib cell line present on plasmids (Helgason et al., 2000). Eighteen B. cereus group genomes have been completely sequenced and published in GenBank. Insertion sequences (ISs) are small transposable DNA fragments consisting of, in general, a unique transposase-encoding gene and terminal inverted repeats (IRs), which serve as the sites Reverse transcriptase for recognition and cleavage by transposases (Tpases) (Mahillon & Chandler, 1998). A large number of ISs have been

classified into 22 families mainly based on the amino acid sequence similarities of their Tpases (Siguier et al., 2006a). ISs played an important role in genome reshuffling and evolution by facilitating horizontal gene transfer and mediating homologous recombination between multiple copies present in a given genome (Mahillon et al., 1999). The diversity and distribution of some well-known ISs that are generally structurally associated with genes coding for parasporal crystal proteins in B. thuringiensis have been widely studied (Mahillon et al., 1994; Leonard et al., 1997; Rosso & Delecluse, 1997; Joung & Cote, 2003; Huang et al., 2004). However, the entire ISs content of the B. thuringiensis genome has never been reported. Bacillus thuringiensis ssp.

The data represent the average change (n-fold) determined from at least three independent experiments. As a control we used the housekeeping gene gapdh, which was carefully validated before its use in quantitative mRNA assays with 16S rRNA gene expression as an internal control obtained under the same conditions and determined

from at least three independent experiments. Growth temperature regulates the production and specificity of CPS in E. coli K92 (González-Clemente et al., 1990; Navasa et al., 2009). We therefore sought to determine whether the genes responsible for capsular metabolism and regulation are modulated at temperatures that represent the mammalian host (37 °C) and at ambient conditions (19 °C). Parallel cultures grown at 37 and 19 °C

in xylose–asparagine defined medium PLX4032 cell line with aeration (González-Clemente et al., 1990; Navasa et al., 2009) were harvested at the exponential phase around 29–31 generations after inoculation. Thus, the results obtained reflect the adapted state and signify genes whose expression is differentially maintained over long-term growth at a given temperature (White-Ziegler et al., 2007). Of the genes studied and that we considered as representative (Fig. 1) and directly involved in the metabolism and/or control of both capsular polymers, 19 were found to be highly expressed at 37 °C (Tables 2–4), whereas nine genes were predominantly expressed at 19 °C (Table 3). The validity of the experimental design is supported by the fact that all genes contained on the kps cluster showed the greatest Resveratrol increase at 37 °C (more Ponatinib datasheet than 500-fold

in the case of the neuE and neuS genes). To analyse expression levels of the genes of the kps cluster, we selected one or more genes of each functional region (Fig. 1a). Because regions 1 and 3 of group 2 capsules are organized in two different transcriptional units (Pazzani et al., 1993; Cieslewicz & Vimr, 1996; Stevens et al., 1997), we studied the expression of the first genes of each region (kpsF and kpsM, respectively) as representatives. We also analysed the expression of all neu genes located on the specific 2 region (Whitfield, 2006). As shown in Table 2, the expression levels of all genes of the kps cluster studied (namely kps of regions 1 and 3 and neu of region 2) were significantly increased at 37 °C compared with at 19 °C (above 15-fold in most cases) while more than a 500-fold increase was observed for the neuE and neuS genes. Higher expression levels were observed in genes belonging to region 2 (neu genes), while expression levels of kpsF (region 1) were lower than those obtained for other genes of the cluster (between five- and 30-fold lower). We also analysed the effect of growth temperature on expression levels of the genes involved in sialic acid catabolism (Kalivoda et al., 2003; Vimr et al., 2004) in E. coli K92 (Fig. 1b).

8-fold increase at 24-h postinfection). This phenomenon is coupled with decreased cell survival (16% survival in A. salmonicida infection vs. 54% of survival in S. iniae cocultured cells at 24-h postinfection). However, meticulous analysis of TNF-α mRNA transcription patterns reveals that, depending on (1) bacterial type and (2) bacterial viability, CHIR-99021 price two substantial quantitative differences in TNF-α

transcription levels can be perceived. First, live bacteria constantly induced higher levels of TNF-α1 and TNF-α2 mRNA expression compared with heat-killed bacteria (16±1.8- vs. 4.1±0.5- or 10.4±1.6-fold increase for A. salmonicida, P<0.01, at 24 h; 3.7±0.2- or 6.6±0.8- vs. 2.5±0.4- or 5.2±0.6-fold increase for S. iniae, P<0.01, at 6 h). Secondly, infection with A. salmonicida, whether live or dead, induced higher TNF-α transcription levels than infection with S. iniae (16±1.8-

or 4.1±0.5- to 10.4±1.6- MEK inhibitor vs. 3.7±0.2- to 6.6±0.8- or 2.5±0.4- to 5.2±0.6-fold increase in TNF-α1 and TNF-α2 transcription levels for live or dead A. salmonicida or S. iniae, respectively; P<0.05 for live bacteria throughout the experiment and P<0.01 for dead bacteria at 9 h). LPS (positive control) stimulation of RTS11 macrophages gave rise to a time-dependent increase of TNF-α transcription levels (5.2±0.8- to 5.7±0.6-fold increase for TNF-α1 and TNF-α2, peaking at 9 h; P<0.001) that resembles bacterial stimulation (Fig. 2). No differences in cytokine expression levels were recorded following PBS stimulation. The overall similarity (both from the kinetic and the quantitative aspects) in the increase of TNF-α transcription patterns following LPS stimulation and the coculture of RTS11 trout macrophages with specific pathogens strengthens the reliability of the experimental model. This is further demonstrated by an additional control, consisting of coculture of RTS11 macrophages with live or killed find more S. caseolyticus KFP 776, a commensal

Gram-positive strain recovered from the skin of a healthy rainbow trout. Staphylococcus caseolyticus induced only a minimal increase in TNF-α1 transcription levels (1.4±0.3- or 1.7±0.2-fold increase after coculture with dead or live bacteria, respectively); induction of TNF-α2 transcription (3.6±0.5- or 4.5±0.6-fold increase after coculture with dead or live bacteria, respectively) was also lower than that of A. salmonicida or S. iniae (P<0.01 for both). The amplitude of IL-1 mRNA transcription levels in RTS11 macrophages stimulated by killed S. iniae cells closely resembled that of the same cells cocultured with LPS or A. salmonicida-positive controls (4.5±0.6, 5.4±0.7 SD and 5.3±0.3-fold increase, respectively; all peaking at 9-h postinfection) (Fig. 1). Interestingly, live S. iniae were found to be poor stimulants of IL-1 mRNA transcription, and the (apparent biwave) rise in IL-1 mRNA transcription levels is notably lower than what was observed with other stimulators (P<0.

Mean DLFs (± SEM) for both stimulation groups from each of the three blocks on both testing days are shown in Fig. 1. Because stimulation was only delivered on the first day, separate 3 (Block) × 2 (Stimulation) mixed-measures anovas were conducted on DLFs in each day. On the first day, mean DLFs rapidly decreased for both groups with training (F2,26 = 5.70, P = 0.009,  = 0.31), showing rapid perceptual learning. DLFs decreased

by 0.95 Hz for the tDCS group and by 0.86 Hz for the sham group. The interaction between Block and Stimulation did not approach significance, offering no evidence of a different rate of learning in the two groups (F2,26 = 1.04, P = 0.36,  = 0.07). DLFs, however, selleckchem were considerably higher in the tDCS than the Z-VAD-FMK chemical structure sham group (F1,13 = 4.84, P = 0.046,  = 0.27). The mean overall DLF for the tDCS group (1.46 Hz) was about double that of the sham stimulation group (0.65 Hz), although both groups improved to a similar extent with training. tDCS therefore degraded frequency discrimination without affecting perceptual learning. Most subjects in the tDCS group showed high DLFs during Block 1 that decreased by Block

2. Some subjects in this group, however, did not show smaller DLFs until Block 3. This variation in the effect of tDCS on auditory cortical functioning most likely caused the greater inter-individual variability of DLFs in the tDCS compared with sham stimulation group as evident in Fig. 1. DLFs in the sham group became asymptotic by the third training block on Day 1 and remained stable on Day 2, whereas DLFs in the

tDCS group returned to near initial levels on Day 2. There was no overall learning effect on Day 2 (F2,26 = 1.22, P = 0.31,  = 0.09). The interaction between Block and Stimulation, however, was significant (F2,26 = 4.20, P = 0.03,  = 0.24). This was due to the sham stimulation having asymptotic DLFs on all blocks whereas DLFs for the tDCS group decreased from Block 4 to 5. DLFs in the group given tDCS on Day 1 were still higher than those for the group given sham stimulation Ribonucleotide reductase on Day 1 (F1,13 = 4.80, P = 0.047,  = 0.27). The overall DLF for the tDCS group (1.19 Hz) was slightly lower than during stimulation on Day 1 but was still about double that of the sham stimulation group (0.59 Hz), showing a persistent effect of tDCS on frequency discrimination. Fig. 2 shows that response times decreased monotonically over training blocks for both groups. Response times for both groups decreased over Blocks on Day 1 (F2,26 = 21.38, P < 0.001,  = 0.62) and Day 2 (F2,26 = 4.88, P = 0.016,  = 0.27). Stimulation did not differentally affect response times with training as the interaction of Stimulation and Block did not approach statistical significance on either Day 1 or Day 2 (both F < 1).

There was a significant correlation between changes in EMG mirroring and the individual maximal s-IHI at baseline (r = 0.65, P = 0.0019; Fig. 6), indicating that the greatest reduction in EMG selleck inhibitor mirroring was associated with the most effective individual maximal s-IHI. The correlation between changes in EMG mirroring and the average baseline l-IHI was not significant (r = 0.25, P = 0.27; Fig. 6). There was no correlation between overall changes in either s-IHI or l-IHI and practice-related changes in EMG mirroring (r = 0.36,

P = 0.11; r = 0.11, P = 0.63). As outlined in the Materials and methods, we also tested whether the practice-related changes in EMG mirroring were related to the changes in acceleration of the ballistic movement or to the changes of the average corticospinal excitability of the trained hemisphere. There was no correlation between changes in EMG mirroring and acceleration peak (r = 0.32, P = 0.16). Similarly, there was no correlation between changes in EMG mirroring and average corticospinal excitability of the trained hemisphere (r = −0.0081,

P = 0.97). In the present study we found that, as reported by others (Classen et al., 1998; Muellbacher et al., 2001; Agostino et al., 2007, 2008), subjects improved performance in the trained task. Furthermore, this happened even though there was no overall change in EMG mirroring, and even a tendency for it to decline. Physiologically there was an increase in the excitability of corticospinal Selleckchem GSK3 inhibitor output from the trained hemisphere, but there was no change in IHI from MTMR9 the trained to the contralateral hemisphere. However, individual changes in EMG mirroring did relate to the basal amount of s-IHI, i.e. the greater the basal levels of s-IHI the greater the reduction in EMG mirroring. The conclusions from this are: (i) that corticospinal excitability and cortico-cortical (interhemispheric) excitability can be modulated independently

by motor training, even though they may share some of the same circuitry (Avanzino et al., 2007); and (ii) basal physiology measures of s-IHI give an indication of the overall extent to which EMG mirroring modification is possible, i.e. that the baseline s-IHI is a key factor that determines how successfully participants can learn to focus their motor commands on the task being trained and prevent overflow to the opposite hemisphere. The reduction in EMG mirroring we observed during motor training in individuals with greater baseline s-IHI was not explained by a change in the level of background EMG activity in the tonically contracting FDIMIRROR as this was constant. Nor is it likely to reflect any fatigue that might have been caused by training as fatigue is known to increase rather than decrease EMG mirroring (Cincotta & Ziemann, 2008). There was also no correlation between the reduced amount of EMG mirroring and the improvement in motor performance, i.e.

This information was then transferred to an electronic spreadsheet and returned to MUSD for analysis. 2071 discharge prescriptions from 45 organisations were audited (1904 from acute trusts; 89 from community health

services; 78 from mental health). 1646 patients (80%) had received a pMR. Pharmacists reported that in 1162 (71%) of these the pMR had helped to ensure that the discharge summary was accurate. In a further 312 prescriptions (19%) the pMR had helped to identify a problem that required resolution. In the remaining 172 prescriptions (10%) it had helped the pharmacist to both identify and resolve a medicines-related issue without the need to contact the prescriber. 377 (18%) of pharmacy contributions were to clarify changes to medicines since admission. Tanespimycin concentration The average time to clinically screen a discharge prescription was 8.7 minutes, and to

CP-868596 resolve identified problems 8.2 minutes. In this service evaluation pharmacists clearly indicated that pMR supported the clinical screening of discharge prescriptions. More detailed review of how discharge prescription accuracy is influenced by pMR is needed, but the results suggest that at minimum pMR helped pharmacists to add information relating to changes to medicines since admission. In 8% of discharges the pMR had removed the need for the pharmacist to contact the prescriber about an identified problem, thus reducing the time required to process the prescription. pMR thus improves medication safety at all points in the patient care pathway. 1. Karnon J, Campbell F, Czoski-Murray C. Model-based cost-effectiveness analysis of interventions Interleukin-2 receptor aimed at preventing medication error at hospital admission (medicines reconciliation). J Eval Clin Prac 2009; 15: 299–306. 2. Dodds L. Unintended discrepancies between pre-admission and admission prescriptions identified by pharmacy-led medicines reconciliation: results of a collaborative

service evaluation across east and South East England. Int J Pharm Prac 2010; 18 (Suppl 2): 9–10. Nicola Gray1, Louise Rosenfield2, Geoffrey Saunders3 1Green Line Consulting Limited, Manchester, UK, 2Prestwich Pharmacy Limited, Manchester, UK, 3The Christie NHS Foundation Trust, Manchester, UK This clinical effectiveness project aimed to explore the adherence of patients to injectable dalteparin upon discharge from a secondary care cancer setting, sometimes supplied under a shared care protocol (SCP), in terms of self-reported adherence rates and factors affecting adherence. Patient and carers encountered challenges to maintaining supplies of injectable dalteparin, including dosage reduction omissions and poor information transfer to GPs. Despite these challenges, participants displayed resilience and determination – during a difficult period – in securing supplies and sustaining good levels of adherence.

aureus virulence in silkworms. Protein A contributes to the virulence of S. aureus by interacting with immunoglobulin in mammalian blood (Palmqvist et al., 2002). The lack of the requirement for spa in S. aureus infection of silkworms is presumably due to the absence of immunoglobulin in invertebrates, including silkworms. We demonstrated that cell-wall-anchored proteins, ClfB, FnbB and Screening Library SdrC, contributed

to the virulence of S. aureus in silkworms. To our knowledge, this is the first report that cell-wall-anchored proteins contribute to the virulence of S. aureus in an invertebrate model animal. ClfB binds cytokeratins of mammalian epithelial cells and the interaction is required for S. aureus colonization onto nasal epithelial cells (Wertheim et al., 2008); FnbB binds mammalian fibronectin and contributes to the virulence of S. aureus (Palmqvist et al., 2005); and SdrC is required for adherence of S. aureus to mammalian epithelial cells (Barbu et al., 2008; Corrigan et al., 2009). Therefore, ClfB, FnbB and SdrC are presumably required Selleckchem Navitoclax for adherence of S. aureus to silkworm tissues

by binding silkworm proteins that are homologous to the mammalian target proteins. Invertebrate animal models of S. aureus infection include C. elegans, D. melanogaster and Manduca sexta, in addition to silkworms (Sifri et al., 2003; Needham et al., 2004; Fleming et al., 2006). In the C. elegans model, bacteria were eaten by worms and the number of surviving worms was counted (Sifri et al., 2003). In the D. melanogaster model, bacteria were injected into adult flies by injuring animals with tungsten needles that were dipped in a solution containing bacteria, and the number of surviving flies was counted (Needham et al., 2004). In the M. sexta model, bacteria were injected into larvae by using microsyringes (Fleming

et al., 2006). In the C. elegans model, the agr locus, saeRS and hla genes of S. aureus are required to kill worms, although srtA is not (Table 3) (Sifri et al., 2003; Bae et al., 2004). In the D. melanogaster model, Guanylate cyclase 2C the agr locus, saeRS and arlRS of S. aureus were not required for killing flies (Table 3) (Needham et al., 2004). In the M. sexta model, the agr locus of S. aureus is involved in killing larvae (Table 3) (Fleming et al., 2006). Our present study revealed that agr, saeRS, arlRS and srtA of S. aureus were required for killing silkworms, whereas hla was not required. The different results between these animal models may be due to different sensitivities of animals against exotoxins, different adhesive characteristics of cell surfaces to bacterial cells, and different experimental conditions, such as temperatures and infection routes. The findings of the present study revealed that genes encoding hemolysins of S. aureus are not required for killing silkworms, whereas some genes encoding cell-wall proteins and regulatory proteins are required.