It’s therefore possible that during the placebo trials participants’ experienced greater levels of muscular fatigue, as evidenced by the reduced mean power output compared to the AOX buy ZD1839 trials, and thus leading to a greater GH response. Further research

is needed to help determine this possibility and the potential role AOX supplementation has on GH secretion. Furthermore, as GH is an anabolic hormone its elevation during RT coupled with appropriate mechanical strain may be important for the process of muscular hypertrophy [51, 52]. This would suggest that the GH results from this study indicate they may be undesirable in regards to promoting muscular hypertrophy. It is therefore of interest for future studies to examine whether this decreased circulating GH would affect muscular hypertrophy after a prolonged period of use or whether it acutely affects IGF-1 levels. Moreover, recent

research suggests excessive AOX supplementation may hinder important physiological training adaptations [3, 53]. This has prompted the suggestion that optimal oxidant content for maximal force production exists within the muscle [53]. These recent findings and the GH results in this study, highlight the need to further our understanding of the effect of AOX supplementation on training adaptations. Conclusions In conclusion, an acute dose of a PYC based AOX supplement enhanced lower body RT performance in trained males by improving mean concentric power, velocity and total PI3K inhibitor work output. The mechanisms involved are still unclear considering oxidative stress response (measured as plasma XO) was not significantly reduced in the AOX treatment, as hypothesised. Future studies should incorporate further measures of oxidative stress, particularly GSH, and muscle Dichloromethane dehalogenase blood flow which may help determine the biochemical and physiological mechanisms that led to the results in this study. Furthermore, GH secretion was significantly attenuated in the AOX trial compared

to the placebo. The mechanisms that led to these results are not fully understood, but further research is required as GH secretion is involved in MH and strength development and its attenuation may negatively impact training adaptations. References 1. Ferreira LF, Reid MB: Muscle-derived ROS and thiol regulation in muscle fatigue. J Appl Phys 2008, 104:853–860. 2. Finaud J, Lac G, Filaire E: Oxidative stress relationship with exercise and training. Sports Med 2006, 36:327–358.PubMedCrossRef 3. Peternelj TT, Coombes JS: Antioxidant supplementation during exercise training beneficial or detrimental? Sports Med 2011, 41:1043–1069.PubMedCrossRef 4. Bloomer RJ, Goldfarb AH, Wideman L, McKenzie MJ, Consitt LA: Effects of acute aerobic and anaerobic exercise on blood markers of oxidative stress. J Strength Con Res 2005, 19:276–285. 5.

2007b; Pavlic et al. 2009a, b; Sakalidis et al. 2011). Cryptic species have also been resolved in several

other pathogenic genera using multigene analysis including Colletotrichum, Fusarium and Phyllosticta (Hyde et al. 2010; Summerell et al. 2010, 2011; Cai et al. 2011; Ko-Ko et al. 2011; Wikee et al. 2011a, b; Damm et al. 2012a, b). Conclusion and future work Our data analysis indicates that the order Botryosphaeriales may comprise more families than the presently accepted Botryosphaeriaceae (Lumbsch and Huhndorf 2010). Clade B could be represented by Phyllostictaceae, while Clade A splits into three major clades, A1-A3. Clade A1 comprises Diplodia, Neodeightonia and Lasiodiplodia and is characterized by dark brown, LY294002 chemical structure septate, striate conidia. Clade A2 comprises Barriopsis, Phaeobotryon and Phaeobotryosphaeria, and characterized by dark to dark brown, aseptate or 2-septate ascospores, with or without an apiculus. Clade A3 includes Auerswaldia, Dothiorella and Spencermartinsia. In these genera the ascospores become brown inside the asci, while the conidia become brown when still attached to the conidiogenous cells. Clade A6 (Botryosphaeriaceae) which includes the family

type (Botryosphaeria dothidea) is characterized by hyaline, aseptate ascospores. We refrain from introducing new families for these clades at this stage until a larger dataset can confirm this. In this paper we have re-examined the type specimens of 15 genera of Botryosphaeriales, collected six new species from Thailand selleck and used 124 Botryosphaeriaceae strains with sequence data to derive a modern treatment for the order. There is however still much research to be carried out with resolution of families and genera, linkage of sexual and asexual morphs and differentiation of cryptic species. Acknowledgments We are grateful to the Directors and Curators of the following

herbaria for the loan of specimens in their keeping: BAFC, Edoxaban BPI, IMI, K (M), LPS, PREM, S and ZT. The Mushroom Research Foundation, Bandoo District, Chiang Rai Province, Thailand is acknowledged for providing postgraduate scholarship support and facilities to JK Liu. Appreciation is extended to the Thailand Research Fund BRG528002 for supporting this work. References Abdollahzadeh J, Goltapeh EM, Javadi A, Shams-Bakhsh M, Zare R, Phillips AJL (2009) Barriopsis iraniana and Phaeobotryon cupressi: two new species of the Botryosphaeriaceae from trees in Iran. Persoonia 23:1–8PubMed Abdollahzadeh J, Javadi A, Goltapeh EM, Zare R, Phillips AJL (2010) Phylogeny and morphology of four new species of Lasiodiplodia from Iran. Persoonia 25:1–10PubMed Adesemoye AO, Eskalen A (2011) First report of Spencermartinsia viticola, Neofusicoccum australe, and N. parvum causing branch canker of citrus in California. Plant Dise 95:770–770 Alves A, Correia A, Luque J, Phillips AJL (2004) Botryosphaeria corticola, sp. nov.

Minor sequence differences were mostly in the intergenic regions with a preference to Small molecule library AT-rich areas,

and were to a large extent SNP transitions (A/G and C/T) or single nucleotide insertions or deletions. The remaining differences were due to small insertions or deletions of 5-6 bp. The largest deletion (15bp) and the lowest sequence homology (86%) were observed in the intergenic region cox1- trnR2 (see Fig. 1). Figure 1 Genetic organization of (a) B. bassiana strain Bb147 and (b) B. brongniartii strain IMBST 95031 mtDNA. Protein-coding genes are marked with black arrows, and all other genes with gray arrows. Introns are shown with white arrows. Arrows indicate transcription orientation. Introns B. bassiana Bb147 contained five and B. brongniartii six introns, contributing to their total mtDNA genome size by 20.3% and 24.7%, respectively. All introns were group-I members, located in rnl, cob, cox1, cox2 and nad1 (Fig. 1; for details on exact positions of insertion and type of intron sub-group see Additional File 1, Table S1). All introns contained ORFs, i.e., the Rps3 homolog within the rnl gene (BbrnlI and BbrrnlI2),

putative GIY-YIG homing endonucleases (BbcobI1, cox2I1 and nad1I1) and the LAGLI-DADG endonuclease (Bbcox1I1 and Bbrcox1I1). The insertion positions of these introns were found to be conserved (identical sequences for at least 10 bp upstream and downstream of the insertion) for all known fungal complete mt genomes examined (36 in total). The only exception was the cox2 intron which was rarely encountered in other fungi. Interestingly, the additional Selleckchem CHIR99021 intron detected in rnl of the B. brongniartii IMBST 95031 mt genome (positions 806-2102 of NC_011194 and Additional File 1, Table S1), was inserted at site not encountered before among the other complete mt genomes, i.e.,

the stem formed in domain II of rnl ‘s secondary structure. The target insertion sequence for the intron was GATAAGGTTG↓TGTATGTCAA and its intronic ORF encoded for a GIY-YIG endonuclease Erlotinib datasheet which shared homology (57% identity at the amino acid level) with I-PcI endonuclease of Podospora curvicolla (Acc. No. CAB 72450.1). Intergenic regions Both mt genomes contained 39 intergenic regions amounting for 5,985 bp in B. bassiana and 5,723 bp in B. brongniartii, and corresponding to 18.6% and 16.9% of their total mt genome, respectively. The A+T content was very similar for these regions in both mt genomes (~74.5%) and the largest intergenic region was located between cox1-trnR2 with sizes 1,314 bp for B. bassiana and 1,274 bp for B. brongniartii, respectively. Analysis of these particular regions revealed large unique putative ORFs (orf387 and orf368 for both genomes) with no significant similarity to any other ORFs in Genbank. Additionally, many direct repeats were also located in the same regions (maximum length 37 bp and 53 bp for B. bassiana and B. brongniartii, respectively).

These results agree with the differences found by Hernández et al. [34], who

analyzed the extracellular activity of pectin lyase in both races of C. lindemuthianum under the same conditions employed in this study. When both races were grown this website with glucose, extracellular PNL activity was barely detected after 8 (race 1472) and 10 (race 0) days of incubation, as observed in this study. Plant cell walls from P. vulgaris induced a similarly low PNL activity in the two isolates after 7-8 days of incubation. When pectin esterified to 92% was used as the carbon source, the activity in the pathogenic race nearly doubled compared with the activity in the non-pathogenic race. Early transcription Selleck MK-8669 of genes encoding lytic enzymes and late detection of the corresponding activities is a well documented phenomenon in different fungi [8, 30, 65, 68]. Apart from the presence of a regulatory system controlling gene expression, the production of active pectinase and probably other lyticases can be modulated by other mechanisms such as postranslational modification and protein transport [69]. These alternatives may help to explain the differences observed in this study. The pectin lyase of the pathogenic race of C. lindemuthianum is able to degrade highly esterified pectin (92%), unlike

that of the non-pathogenic race. Apparently, the differences between the pathogenic and non-pathogenic Montelukast Sodium races of C. lindemuthianum occur as much at the expression level as at the level of enzymatic activity, and it is clear that the non-pathogenic and pathogenic races of C. lindemuthianum respond of different form to the carbon sources (except for glucose, where the mRNA of Clpnl2 and the active enzyme is synthesized at basal levels). It has been proposed that the basal level of enzymatic activity breaks down the substrate, generating degradation products that further induce enzymatic activity [64]. A similar behavior has been

observed in our laboratory for other enzymes that degrade cell walls, such as cellulases and the xylanase and β-xylosidase of C. lindemuthianum (unpublished data). Several studies have reported that the pectinolytic enzymes play an important role in pathogenesis [70, 71]. These are the first enzymes that act during the infection of the plant, causing extensive degradation of the cell wall and the main symptoms of the disease [72]. However, in addition to enzyme production, the sequence in which the enzymes are produced, the speed of synthesis, concentration and diffusion of enzyme are also fundamental aspects of the pathogenesis process [72]. The non-pathogenic race of C. lindemuthianum used in this work is unable to infect P. vulgaris, and thus its lifestyle is closer to that of a saprophytic fungus.

Our quantitative analyses showed that the respective activities of metallo- and serine proteinases in gardens of higher attine ants (including the leaf-cutting ants) tend to be negatively correlated (Figure 1). In most symbionts, the split is very pronounced, with almost complete specialization on one of the two classes of proteinases, although the symbiont of T. cornetzi colony 17 is an exception showing almost equal, intermediate activities of the two proteinase classes. This suggests that there may be a trade-off in the expression of proteinases and that there may be adaptive reasons of substrate processing

that make the production of either serine- or metalloproteinases most appropriate. Both serine proteinases and metalloproteinases are very widespread in nature and are involved in a wide variety of biological PD-0332991 molecular weight processes. Enzymes belonging

to these classes vary significantly in substrate specificity which may correspond to the requirements of fungal ecological niches [36]. One explanation for the shift towards almost exclusive serine proteinase activity might therefore be that the ants that rear these symbionts forage for leaf and flower material that can be more effectively degraded by serine proteinases [37]. Recent studies by Mikheyev et Selleckchem Galunisertib al. [38, 34] have shown that North American aminophylline Trachymyrmex rear at least four different species of fungal symbiont, whereas virtually all leaf-cutting ants throughout Latin America appear to rear a single species (Leucocoprinus gongylophorus (Möller) (http://​www.​indexfungorum.​org), which has likely been derived secondarily no longer than 2-3 million years ago and swept horizontally through most if not all species of Acromyrmex and Atta leaf-cutting ants, who themselves had their last common ancestor 8-12 million years ago [39]. Whether this selective sweep had

any connection with the symbiont being a strain with upregulated activity of metalloproteinases is presently unknown, but it would be of interest if rare leaf-cutting ants could be found that rear gardens that are more closely related to the serine protease producing Trachymyrmex and Sericomyrmex symbionts. We have so far assumed that the measured proteinase activities originate from enzymes produced by the fungal symbiont of the ants. They could also possibly originate from the additional microorganisms found in the fungus gardens of attine ants [40–42]. However, as earlier mentioned [25], the fungal symbiont comprises by far the largest microbial biomass fraction of gardens, so that contributions from other microorganisms should be quantitatively negligible unless they would be specialized symbionts selected for specific enzyme production (for which there is no indication so far).

J Steroid Biochem Mol Biol 1996, 57:203–213.PubMedCrossRef 4. Berry DA, Cirrincione C, Henderson IC, Citron ML, Budman DR, Goldstein LJ, Martino S, Perez EA, Muss HB, Norton L, et al.: Estrogen-receptor status and outcomes of modern chemotherapy for patients with node-positive Selleck STA-9090 breast cancer. JAMA 2006, 295:1658–1667.PubMedCrossRef 5. Colleoni M, Minchella I, Mazzarol G, Nole F, Peruzzotti G, Rocca A, Viale G, Orlando L, Ferretti G, Curigliano G, et al.: Response to primary chemotherapy

in breast cancer patients with tumors not expressing estrogen and progesterone receptors. Ann Oncol 2000, 11:1057–1059.PubMedCrossRef 6. Petit T, Wilt M, Velten M, Rodier JF, Fricker JP, Dufour P, Ghnassia JP: Semi-quantitative evaluation of estrogen receptor expression is a strong predictive factor of pathological complete response after anthracycline-based neo-adjuvant chemotherapy in hormonal-sensitive breast cancer. Breast Cancer Res Treat 2010, 124:387–391.PubMedCrossRef 7. Stearns V, PLX3397 mw Singh B, Tsangaris T, Crawford JG, Novielli A, Ellis MJ, Isaacs C, Pennanen M, Tibery C, Farhad A, et al.: A prospective randomized pilot study to evaluate predictors of response in serial core biopsies to single agent neoadjuvant doxorubicin or paclitaxel for patients with locally advanced breast cancer.

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to three different chemotherapy regimens: a case control study. BMC Cancer 2009, 9:226.PubMedCrossRef 10. Lee HH, Zhu Y, Govindasamy KM, Gopalan G: Downregulation of Aurora-A overrides estrogen-mediated growth and chemoresistance in breast cancer cells. Endocr Relat Cancer 2008, 15:765–775.PubMedCrossRef 11. Sui M, Huang Paclitaxel concentration Y, Park BH, Davidson NE, Fan W: Estrogen receptor alpha mediates breast cancer cell resistance to paclitaxel through inhibition of apoptotic cell death. Cancer Res 2007, 67:5337–5344.PubMedCrossRef 12. Sui M, Jiang D, Hinsch C, Fan W: Fulvestrant (ICI 182,780) sensitizes breast cancer cells expressing estrogen receptor alpha to vinblastine and vinorelbine. Breast Cancer Res Treat 2010, 121:335–345.PubMedCrossRef 13. Tabuchi Y, Matsuoka J, Gunduz M, Imada T, Ono R, Ito M, Motoki T, Yamatsuji T, Shirakawa Y, Takaoka M, et al.: Resistance to paclitaxel therapy is related with Bcl-2 expression through an estrogen receptor mediated pathway in breast cancer. Int J Oncol 2009, 34:313–319.PubMed 14. Teixeira C, Reed JC, Pratt MA: Estrogen promotes chemotherapeutic drug resistance by a mechanism involving Bcl-2 proto-oncogene expression in human breast cancer cells. Cancer Res 1995, 55:3902–3907.PubMed 15.

Boyd SD. Management of HIV infection in treatment-naive patients: a review of the most current recommendations. Am J Health Syst Pharm.

2011;68:991–1001.PubMedCentralPubMedCrossRef 2. Whitney JB, Lim SY, Wainberg MA. Evolutionary mechanisms of retroviral persistence. AIDS Rev. 2011;13:234–9.PubMed 3. Wainberg MA, Zaharatos GJ, Brenner BG. Development of antiretroviral drug resistance. N Engl J Med. 2011;365:637–46.PubMedCrossRef 4. Gupta RK, Jordan MR, Sultan BJ, Hill A, Davis DH, Gregson J, Sawyer AW, Hamers RL, Ndembi N, Pillay D, Bertagnolio S. Global trends in antiretroviral resistance in treatment-naive individuals with HIV after rollout of antiretroviral treatment in resource-limited settings: a global collaborative study and meta-regression analysis. Lancet. 2012;380(9849):1250–8.PubMedCentralPubMedCrossRef 5. Blanco JL, Varghese Talazoparib V, Rhee SY, Gatell JM, Shafer RW. HIV-1 integrase inhibitor resistance and its clinical implications. J Infect Dis. 2011;203:1204–14.PubMedCentralPubMedCrossRef 6. Mesplede

T, Quashie PK, Wainberg MA. Resistance to HIV integrase inhibitors. Curr Opin HIV AIDS. 2012;7(5):401–98.PubMedCrossRef 7. Wainberg MA, Mesplede T, Quashie PK. The development of novel HIV integrase inhibitors and the problem of drug resistance. Curr Opin Virol. 2012;2:656–62.PubMedCrossRef 8. Quashie PK, Mesplede T, Wainberg MA. HIV drug resistance and the advent of integrase inhibitors. Curr Infect Dis Rep. 2012;15(1):85–100.CrossRef 9. Orkin C, DeJesus E, Khanlou H, Stoehr A, Supparatpinyo K, Lathouwers E, Lefebvre E, Opsomer triclocarban M, Van de Casteele T, Tomaka F. Final 192-week efficacy Barasertib and safety of once-daily darunavir/ritonavir compared with lopinavir/ritonavir in HIV-1-infected treatment-naive patients in the ARTEMIS trial. HIV Med. 2013;14:49–59.PubMedCrossRef 10. Kempf DJ, King MS, Bernstein B, Cernohous P, Bauer E, Moseley J, Gu K, Hsu A, Brun S, Sun E. Incidence of resistance in a double-blind study comparing lopinavir/ritonavir plus stavudine and lamivudine to nelfinavir plus stavudine and lamivudine. J Infect Dis. 2004;189:51–60.PubMedCrossRef 11. Walmsley S, Bernstein B, King M, Arribas J, Beall G, Ruane P, Johnson M, Johnson

D, Lalonde R, Japour A, et al. Lopinavir–ritonavir versus nelfinavir for the initial treatment of HIV infection. N Engl J Med. 2002;346:2039–46.PubMedCrossRef 12. Llibre JM. First-line boosted protease inhibitor-based regimens in treatment-naive HIV-1-infected patients—making a good thing better. AIDS Rev. 2009;11:215–22.PubMed 13. Adams J, Patel N, Mankaryous N, Tadros M, Miller CD. Nonnucleoside reverse transcriptase inhibitor resistance and the role of the second-generation agents. Ann Pharmacother. 2010;44:157–65.PubMedCrossRef 14. Puras Lutzke RA, Eppens NA, Weber PA, Houghten RA, Plasterk RH. Identification of a hexapeptide inhibitor of the human immunodeficiency virus integrase protein by using a combinatorial chemical library. Proc Natl Acad Sci USA.

Interestingly, the highly conserved serine threonine-kinase of S. pneumoniae is thus involved in the processes underlying three key features of bacterial physiology and PLX4032 in vitro evolution: virulence in animals, development of competence for genetic transformation culminating in gene transfers [7], and susceptibility to penicillin (this work). This makes StkP a potentially promising target in S. pneumoniae for the development of new prophylactic measurements against pneumococcal

disease. Conclusion In summary, the results of the present study suggest that pneumococcal serine-theonine kinase (StkP) is related to penicillin susceptibility, as demonstrated in isogenic strains. However, is a highly conserved protein, not functionally related to the major genetic determinants for penicillin susceptibility in pneumococci, being a promising target for the development of new therapies. Acknowledgements R. Dias

was supported by grant BIC 03.2002 from NIH Dr. Ricardo Jorge and was Selleckchem Crizotinib the recipient of a short-term research fellowship grant from the Fundação Calouste Gulbenkian. The authors thank Tania Arcondeguy for her critical reading of the manuscript and suggestions. Electronic supplementary material Additional file 1: Data Tables. Data tables. This file contains table ST1 for the deduced amino acid substitutions in StkP and related PBP profiles of 50 clinical strains and 6 reference as well as tables ST2, ST3 and ST4 for the deduced amino acid substitutions in PBP2B; PBP2X and PBP1A, respectively, of 25 representative pneumococcal strains. (PDF 358 KB) References 1. Filipe SR, Tomasz A: Inhibition of the expression of penicillin resistance in Streptococcus pneumoniae by inactivation of cell wall muropeptide branching genes. Proc Natl Acad Sci USA 2000, 97:4891–4896.CrossRefPubMed 2. Guenzi E, Gasc AM, Sicard MA, Hakenbeck R: A two-component signal-transducing

system is involved in competence and Pregnenolone penicillin susceptibility in laboratory mutants of Streptococcus pneumoniae. Mol Microbiol 1994, 12:505–515.CrossRefPubMed 3. Hakenbeck R, Grebe T, Zahner D, Stock JB: Beta-lactam resistance in Streptococcus pneumoniae : penicillin-binding proteins and non-penicillin-binding proteins. Mol Microbiol 1999, 33:673–678.CrossRefPubMed 4. Mengin-Lecreulx D, van Heijenoort J: Characterization of the essential gene glmM encoding phosphoglucosamine mutase in Escherichia coli. J Biol Chem 1996, 271:32–39.CrossRefPubMed 5. Jolly L, Ferrari P, Blanot D, Van Heijenoort J, Fassy F, Mengin-Lecreulx D: Reaction mechanism of phosphoglucosamine mutase from Escherichia coli. Eur J Biochem 1999, 262:202–210.CrossRefPubMed 6.

aureus Δsfa parental strain (Figure 1D). Supplementation of growth media with L-Dap bypasses sbnA and sbnB mutations, allowing for restored staphyloferrin B production in S. aureus If SbnA and SbnB are involved in the production of L-Dap for staphyloferrin B biosynthesis, then the growth deficit phenotype displayed by S. aureus Δsfa sbnA::Tc and S. aureus Δsfa sbnB::Tc mutants (Figure 1) should be restored when L-Dap is supplemented in the culture medium, since presence of this molecule would bypass the need for the activities of SbnA or SbnB in siderophore production. Accordingly, as shown in Figure 2A, the iron-restricted growth of sbnA and

sbnB https://www.selleckchem.com/products/lgk-974.html mutants is restored equivalent to that of staphyloferrin B-producing cells when the culture medium of the sbnA and sbnB mutants is supplemented with L-Dap, but not D-Dap. This is in agreement with the fact that only the L-isomer of Dap is present in the final structure of the staphyloferrin B molecule [15, 16, 28]. Providing L-Dap to the complete staphyloferrin-deficient mutant (Δsfa Δsbn) did not allow iron-restricted growth, suggesting that growth restoration of sbnA and sbnB mutants by L-Dap is a INK 128 purchase result of this precursor being incorporated into a functional siderophore in the presence of other staphyloferrin B biosynthesis enzymes (Figure 2A).

This result shows that provision of L-Dap to either sbnA or sbnB mutants allowed the bypass of the requirement for these genes in staphyloferrin B biosynthesis, which strongly supports the hypothesis that sbnA and sbnB function together in a direct role in L-Dap synthesis.

Figure 2 Supplementation of culture medium with L-Dap allows S. aureus sbnA and sbnB mutants to overcome the block in synthesis of staphyloferrin B. A) Bacterial growth curves in chelex 100-treated TMS containing 10 μM holo-transferrin as the sole iron source, with the indicated supplements. B) Siderophore Obatoclax Mesylate (GX15-070) quantification from culture supernatants of iron-starved S. aureus mutants via CAS assay (see Materials and Methods). The inset graph represents culture supernatants from identical strains but grown in medium supplemented with FeCl3. Siderophore units are normalized to culture density. C) Same as in B) except culture media was supplemented with L-Dap. D) Siderophore-disk diffusion assays. Culture supernatants to be tested were derived from S. aureus Δsfa sbnA::Tc or Δsfa sbnB::Tc strains cultured in medium supplemented with, or without, L-Dap, as indicated, and were spotted onto sterile paper disks before being placed onto TMS agar plates seeded with S. aureus wild-type and siderophore transport mutants, as indicated. Plate disk bioassay is described in Materials and Methods. E) Bacterial growth curves for cultures of S. aureus Δsfa sbnA::Tc and S.

Depth of coverage was generally consistent, apart from two contigs which showed 3.5

times greater-than-average coverage. Scrutiny of the larger of these two contigs (9.4 kb) identified CDSs that are predicted to encode plasmid replication and mobilization proteins. This contig also contains homologs of sul1 and uspA genes, which are often associated with A. baumannii resistance islands [41]. A. lwoffii NCTC 5866 genome characteristics A. lwoffii was first described by Audureau in 1940 under the name Moraxella lwoffii[22], but was later moved to genus Acinetobacter by Baumann et al.[23]. In 1986, Bouvet and Grimont emended the description of the species to designate strain NCTC 5866 the type strain

[42]. We identified 3005 good-quality CDSs in the NCTC 5866 genome, of which 229 do not have Dabrafenib homologs in any of the Acinetobacter genomes examined see more in this study. Investigation of these CDSs revealed two putative prophages, ca. 44.5 and 25.6 kb. Interestingly, many of the CDSs found in these two putative prophages are also present in a recently sequenced environmental Acinetobacter strain P8-3-8 (not included in this study) isolated from the intestine of a blue-spotted cornetfish caught in Vietnam [43]. Among the remaining strain-specific CDSs, we identified fourteen that are nearly identical to tra genes found in PHH1107, a low GC content plasmid isolated from pig manure [44]. The tra homologs are distributed on two contigs, one of which has a GC content (37%) lower than the genome mean (43%). A. parvus DSM 16617 genome characteristics Carbohydrate Strain DSM 16617 is the type strain for A. parvus isolated from the ear of an outpatient from Pribram, Czech Republic in 1996 [45]. We identified 2681 good-quality CDSs in the DSM 16617 genome,

179 of which do not have homologs in any of the remaining 37 genomes. Analysis with Prophinder [46] identified one 39kb putative prophage containing phage-related genes homologs to putative phage-related genes found in A. baumannii and A. oleivorans DR1. We identified an 8kb contig with 2.5 times higher than average depth of coverage, which contains homologs to phage related genes. A. bereziniae LMG 1003 genome characteristics Strain LMG 1003 is the type strain for A. bereziniae, a recently named species by Nemec et al., which has been isolated from various human, animal and environmental sources [47]. We identified 4480 good-quality CDSs in the genome, with 1061 strain-specific CDSs (no homologs in the rest of the 37 genomes). This is a considerably higher percentage, 24%, than in other Acinetobacter strains (see Additional file 1). Many of the strain-specific CDSs form clusters of four or more CDSs, with the largest cluster containing 49 consecutive CDSs, of which 45 are strain-specific.