Discussion The etiology of gastric cancer is selleckchem multifactorial, multigenetic and multistage [24, 25]. It is known that during carcinogenesis, TGF-β can switch from a tumor suppressor to a tumor enhancer in the later stages of cancer [26]. With dual role in cancer development, there is great interest in analyzing the role of genetic variation in TGFB1 in cancer progression and patient survival. For example, the TGFB1 -509C>T and rs1982073 (or rs1800470) polymorphisms have

been shown to be associated with breast cancer survival in a Chinese population [27–30] and chemoradiotherapy response in 175 Finnish patients with head and neck squamous cancer[31], respectively. However, neither TGFB1 QNZ in vivo +869T>C nor +915G>C polymorphisms showed any association with tumor relapse and progression in bladder tumors without muscular invasive in a Spanish population [32]. While a Korean study showed that the variant T genotypes of the TGFB1 -509C>T SNP were associated with a reduced risk of lung cancer [33], a Chinese Epoxomicin study of 414 patients and 414 controls [34] reported that the genotypes were not associated with an overall risk of developing gastric cancer but with a decreased risk of risk of stage I or II gastric cancer.

However, no survival analyses were presented Silibinin in these studies. As noted, we did not find any statistical evidence to support a significant association between TGFB1 polymorphisms and overall survival in gastric cancer. However, the significant association between TGFB1+ 915 CG/CC genotypes and 2-year survival for all gastric cancer patients suggests that this TGFB1 variant may have attenuated the role of TGF-β1 as a tumor suppressor in the earlier stage of tumor progression. It is also known that TGF-β1 can switch from a tumor

suppressor to a tumor enhancer in the late stage of cancer [26]. Once the tumors had grown bigger and become metastatic, the resultant increase in somatic mutations or gains in the copies of oncogenes may have outweighed the role of the suppressor variants in the late stages of the tumor, leading to no difference in overall survival of the patients with different genotypes of the TGFB1+ 915 G>C SNP. However, this speculation needs to be validated in more rigorously designed studies with a much larger sample size and more information on the mutation spectrum in the tumors. VEGF, as a key mediator of angiogenesis, also plays an important role in the development of cancers. VEGF polymorphisms have also been shown to be associated with survival in both gastric cancer and colorectal cancer [35, 36]. However, the results from published studies remain inconsistent rather than conclusive.

The ubiquitin–proteasome pathway is the most important mechanism for protein degradation in skeletal muscle cells. This system involves a series of enzymatic steps in which the degraded proteins are first targeted by an enzyme system that binds the target protein to the polypeptide ubiquitin. These ubiquitinized proteins are then transferred to the proteasome complex and degraded into short peptides and are finally recycled as free intracellular amino acids [42].

AZD1390 supplier This pathway is promoted by inflammatory cytokines such as tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6), by hormones such as cortisol and angiotensin, as well as by reactive oxygen species. Increased expression of these inflammatory cytokines also appears to be common in aging in skeletal muscle. Comparison of skeletal muscle biopsies from younger and older subjects showed increased expression of genes upregulated by inflammatory factors [43]. Levels of catabolism-inducing

hormones such as cortisol have also been shown to increase with age, and cortisol is linked to increased expression of IL-6 and TNF-α. Increased TNF-α expression is also known to stimulate muscle atrophy through apoptosis. Apoptosis contributes to the loss of myonuclei in skeletal muscle cells and could theoretically result in the loss of complete fibers in sarcopenia [44]. Oxidative damage Oxidative metabolism generates reactive oxygen species (ROS), and these metabolic products are thought to accumulate over time, altering and damaging cell Tideglusib price components, particularly mitochondria and DNA sequences [45]. Because mitochondria produce ROS, they are subject to alterations in their structure

and in their DNA. Alterations to mtDNA are known to increase with age in skeletal muscle, and the frequency of abnormal FHPI mitochondrial Acetophenone regions is higher in those muscles which are strongly affected by sarcopenia [45–47]. The role of mitochondrial DNA alterations in age-related loss of skeletal muscle function is under intense investigation, focusing on their roles in causing skeletal muscle cell apoptosis and structural abnormalities that affect metabolic function. Structural alterations to mitochondria may affect the electron transport chain, compromising respiration. Although the loss of maximal oxygen consumption (VO2 max) with age has been primarily attributed to loss of muscle mass and reduced cardiac output, altered mitochondrial metabolism, leading to poorer muscle cell respiration, may also be involved. Intrinsic changes to skeletal muscle One potential mechanism for sarcopenia involves the loss of muscle regenerative capacity due to loss in the number and function of muscle satellite cells, which proliferate and differentiate into skeletal muscle fibers.

Insulating properties of alumina prevent any gold deposition on the AAO template. Native silicon oxide can also interfere with gold deposition in the nanopores by blocking the electron flow from the substrate to the electrolyte. A deoxidation using vapor HF etching is therefore undertaken before catalyst deposition to remove any traces of native oxide at the bottom of every pores of the template, thus improving gold deposition yield. (1) Figure 1 Controlling the geometry of the AAO template. (a) Periodicity of the nanopore array can be learn more adjusted by varying the anodization voltage and the acid used.

(b) Diameter of the nanopores is controlled by a chemical etching in phosphoric acid (7 wt.%, 30°C), the plot is for a 40-V alumina. Subsequently, silicon nanowire growth is performed MEK inhibitor in a commercial hot-wall low-pressure CVD reactor. A flux of 50 sccm of silane (SiH4) carried by 1,400 sccm of hydrogen (H2) is injected at 580°C under a pressure of 3 Torr. It is known that these experimental conditions allow the diffusion of silane towards the bottom of the pores [19, 22], therefore enabling nanowires’ growth. Addition

of gaseous hydrogen chloride during growth [23] Akt activator is crucial because it prevents the gold catalyst from diffusing on alumina and escaping from the nanopores, which would lead to the growth of silicon nanowires on the top of the AAO template in an uncontrolled way. Growth is carried out for 25 to 35 min depending on the AAO thickness, long enough to let the wires grow out of

the template. After growth, the samples are therefore constituted of a silicon substrate with an AAO template filled with silicon nanowires. The nanowires, which grew out of the template, present neither organization nor constant diameter as can be seen on the scanning electron microscope (SEM) picture of Figure 2a. Indeed, when nanowires reach the surface of the AAO, growth conditions change abruptly leading to kinks in their growth direction. Besides, the density of circular nanopores is so high that the catalyst droplets of two or more adjacent nanowires are close enough to merge and form a bigger single droplet, leading to the growth Liothyronine Sodium of a larger diameter nanowire. To remove these unorganized outer nanowires, samples are sonicated for 1 min in IPA. Ultrasonic vibrations break the nanowires close to their interface with the AAO template. The surface of the nanowire array turns clean, and the only remaining structures coming out of the AAO are a few nanometers of silicon nanowires (Figure 2b). After this step, we also notice the presence of nanowires which just reached the surface of the AAO and did not grow out of it. Their catalyst droplets are at the interface with free space, sometimes merging with other ones to produce the larger diameter nanowires noticed in Figure 2a.

Acknowledgements In memoriam of the Professor Gustavo Linares-Cruz (1956-2005). (*) PF and LV have equally contributed

to this article and must be considered as 2nd authors and M-PP and DP as 3rd authors. We thank Dr M. Mate (Uruguay) for surgical procedures, Dr. J. Carzoglio (Uruguay) for histological evaluation of the breast tumors and Dr Susan Powell for manuscript corrections. This work was supported by the action U03S03 from the ECOS-Sud program (France-Uruguay). Comisión Honoraria de Lucha Contra el Cáncer (CHLCC), Uruguay. References 1. Carthew RW, Rubin GM: Seven in absentia, a gene required for specification of R7 cell fate in the Drosophila eye. Cell 1990, 63:561–77.PubMedCrossRef 2. Hu G, Fearon ER: Siah-1 N-terminal RING domain is required for proteolysis function, and C-terminal eFT-508 order sequences regulate oligomerization and binding to target proteins. Mol Cell INCB28060 cost Biol 1999,19(1):724–32.PubMed 3. Germani A, Bruzzoni-Giovanelli H, selleck chemical Fellous A, Gisselbrecht S, Varin-Blank N, Calvo F: SIAH-1 interacts with α-tubulin and degrades the kinesin Kid by proteasome pathway during mitosis. Oncogene 2000, 19:5997–6006.PubMedCrossRef 4. Santelli E, Leone M, Li C, Fukushima T, Preece NE,

Olson AJ, Ely KR, Reed JC, Pellecchia M, Liddington RC, Matsuzawa S: Structural analysis of Siah1-Siah-interacting protein interactions and insights into the assembly of an E3 ligase multiprotein complex. J Biol Chem 2005,280(40):34278–87.PubMedCrossRef 5. Nemani M, Linares-Cruz G, Bruzzoni-Giovanelli H, Roperch JP, Tuynder M, Bougueleret L, Cherif D, Medhioub M, Pasturaud P, Alvaro V, der Sarkissan H, Cazes L, Le Paslier D, Le Gall I, Israeli D, Dausset J, Sigaux F, Chumakov I, Oren M, Calvo F,

Methane monooxygenase Amson RB, Cohen D, Telerman A: Activation of the human homologue of the Drosophila sina gene in apoptosis and tumor suppression. Proc Natl Acad Sci USA 1996,93(17):9039–42.PubMedCrossRef 6. Hu G, Zhang S, Vidal M, Baer JL, Xu T, Fearon ER: Mammalian homologs of seven in absentia regulate DCC via the ubiquitin-proteasome pathway. Genes Dev 1997,11(20):2701–14.PubMedCrossRef 7. Zhang J, Guenther MG, Carthew RW, Lazar MA: Proteasomal regulation of nuclear receptor corepressor-mediated repression. Genes Dev 1998, 12:1775–80.PubMedCrossRef 8. Boehm J, He Y, Greiner A, Staudt L, Wirth T: Regulation of BOB.1/OBF.1 stability by SIAH. EMBO J 2001, 20:4153–62.PubMedCrossRef 9. Tiedt R, Bartholdy BA, Matthias G, Newell JW, Matthias P: The RING finger protein Siah-1 regulates the level of the transcriptional coactivator OBF-1. EMBO J 2001, 20:4143–52.PubMedCrossRef 10. Tanikawa J, Ichikawa-Iwata E, Kanei-Ishii C, Nakai A, Matsuzawa S, Reed JC, Ishii S: p53 suppresses the c-Myb-induced activation of heat shock transcription factor 3. J Biol Chem 2000,275(20):15578–85.PubMedCrossRef 11.

g. Liu et al. 2009; Löytynoja and Goldman 2009) may contribute to the resolution of the major problematical nodes in the phylogeny of basidiomycetes and provide insight into its morphological, ecological and functional evolution. For instance, genome-based analyses may well resolve the backbone of the Agaricomycotina phylogeny and elucidate the diversity and evolution of the white rot and brown rot wood-decaying modes and shifts among hosts. 3) Biogeographic inference   In comparison

to plant or animal biogeography, biogeography of fungi is at its very young stages. For instance, understanding of the role of long distance dispersal of spores in the maintenance of fungal species cohesion is in its infancy. Some data suggest that fungal spores are seldom dispersed for Selleck Salubrinal distances greater than 100 m indicating that despite rare long distance dispersal events, significant gene flow via spore dispersal even between islands within Hawaii is quite unlikely

(Bergemann and Miller 2002; Burnett 2003), while others suggests that a single fungal species can sustain appreciable gene flow across virtually global distributions (James et al. 2001; Petersen and Hughes 2007). Biogeographic studies in fungi were impeded by the poor knowledge concerning the accurate distribution of fungal species. Up to now, biogeography of diverse groups of basidiomycetes is still very speculative and is only supported by fragmentary observations. Studies based only on morphological characters may provide a very incomplete isometheptene Enzalutamide manufacturer and oversimplified picture of distribution patterns and associated historical events (Wu et al. 2000). Many intriguing morphological similarity based geographic distribution patterns, such as the well-known “Asa Gray disjunction” or a vicariance pattern in the Grayan distribution, and the Gondwanan distribution observed in the past (e.g. Horak 1983; Redhead 1989; Halling 2001; Mueller et al. 2001; Yang 2005b; Petersen and Hughes 2007), could well be inferred by molecular phylogenetic analyses in order to provide a much better understanding of their origin, historical biogeography and dispersal. A more detailed and accurate understanding

of the origin and evolution of a few selected groups of basidiomycetes have been revealed in the last few years, and are compelling areas for future research. For instance, through analyses of ITS and 26S rDNA sequences, and mt-ssu rDNA, Hibbett (2001) demonstrated that there are two main clades of the genus Lentinus, one in the New World, the other in the Old World. The Old World/New World disjunction could be due to fragmentation of an ancient Laurasian range. An alternative Gondwanan hypothesis is not supported by the molecular clock age estimates. Only one long distance dispersal event must be invoked in MM-102 chemical structure Lentinula, that being between Australia and New Zealand. Despite having airborne spores, long distance dispersal is rare in Lentinula. Aanen et al.

Besides, no absorption bands of Si-H stretching mode in the 2090 to 2200 cm−1 spectral domain were detected because of our synthesis methods involving no hydrogen. Since the latter band is generally the most intense Si-H vibration mode

observed in SiN x :H, one can then conclude on the absence of the Si-H wagging (630 to 650 cm−1) and asymmetric stretching (840 to 900 cm−1) modes in the spectra [24, 25, 27, 32–34]. In the same #VX-770 manufacturer randurls[1|1|,|CHEM1|]# manner, no absorption bands of N-H stretching mode were detected in the 3320 to 2500 cm−1 spectral region suggesting that the N-H bending (1140 to 1200 cm−1) modes are also absent in our spectra [24, 25, 32, 33]. As a consequence, the 833-cm−1 band and the 1115-cm−1 shoulder can be unambiguously assigned to the transverse (TO) and the longitudinal (LO) modes of the asymmetric Si-N stretching vibration, respectively [24, 33–37]. The TO-LO SRT2104 splitting is due to the Berreman effect [38] according to which only the TO mode is IR active in normal incidence, and the shoulder observed

with an incidence angle of 65° corresponds to the LO mode. Then, the analysis of the FTIR spectra in the 700 to 1200 spectral domain is particularly interesting since it definitely concerns the Si-N bonding alone, in contrast to many works on the FTIR study of SiN x :H films [5, 27, 32–34, 39], Si nitride layers containing oxygen [19, 20], or SiN x layers stacked between Si oxide layers [17, 40]. Figure 4 FTIR spectra of a SiN x thin film. The films were deposited by the N2-reactive method recorded with a normal incidence and with an incidence angle of 65°. The inset shows the TO and LO band positions of SiN x layers deposited by the N2-reactive (full squares) and the co-sputtering (empty squares) methods as a function of the composition. Figure 5 shows the evolution of the FTIR spectra of SiN x thin films measured with the two incidence angles. The spectra are arranged with nearly increasing

order of n of SiN x films deposited by both methods. One can notice that the evolution of the FTIR spectra is not influenced by the deposition method but only by the composition. The spectra in Figure 5a showing the TO band only change slightly with n, whereas the evolution of the spectra in Figure 5b is more pronounced because of the significant blueshift of the LO band and the concomitant increase of its intensity with decreasing n. The TO band shifts to higher wavenumbers as well but with a lesser extent. Figure 5 Evolution of the FTIR spectra of SiN x with the refractive index. The FTIR spectra of the layers deposited by the N2-reactive (black) and the co-sputtering (gray) methods were measured with a normal incidence (a) and with an incidence angle of 65° (b). Similar blueshifts of the TO band [5, 25, 27, 32–34] and of the LO band [24, 27, 33] were also observed in SiN x :H films. Lucovsky et al. [32] explained the TO band blueshift by the incorporation of H.

A. Primer extension analysis identified at least two major transcriptional start sites for the nan operon. Two bands were present for TS-2 nan as indicated. B. Primer extension identified one start site for the siaPT operon. C. Schematic diagram of the nan and siaPT promoters. Binding sites for SiaR (red box) and CRP (blue box) are indicated as well as putative

-10 boxes for TS-1 nan and TS-1 siaPT (yellow boxes). Glucosamine-6-phosphate is a co-activator for SiaR Previous studies found limited activation of SiaR-regulated operons by sialic acid [14]. The potential for intermediates in the sialic Momelotinib order acid catabolic pathway to influence regulation by SiaR was explored. H. influenzae is unable to transport any of the intermediate sugars or phosphosugars of the sialic acid catabolic pathway [13, 18], therefore

a mutagenesis strategy was necessary. Each gene encoding an enzyme in the catabolic pathway was deleted in an adenylate cyclase (cyaA) mutant strain, resulting in a series of double mutants. The ΔcyaA mutant strain was used to allow for CRP to be activated ML323 chemical structure only by the addition of cAMP in subsequent experiments. In each mutant, sialic acid can be catabolized, but the sugar or phosphosugar immediately upstream of the inactivated enzyme should accumulate (Figure 1B). The mutants were grown to early exponential phase and then either sialic acid, cAMP, or both were added. Expression levels of nanE and siaP, the first genes of the catabolic and transport operons, respectively, were compared using real time Astemizole quantitative RT-PCR (qRT-PCR). RNA from a EPZ-6438 research buy culture that received neither sialic acid nor cAMP served as a reference for each experiment. When both sialic acid and cAMP were added to cultures, expression of nanE was only moderately affected in strains 2019ΔcyaA, 2019ΔcyaA ΔnanK, 2019ΔcyaA ΔnanA, and 2019ΔcyaA ΔnagA (0.7- to 5-fold change). The most striking change in nanE expression occurred in 2019ΔcyaA ΔnagB, with expression elevated 83-fold (Fig, 3). This mutant would be unable to convert GlcN-6P to fructose-6P, thus accumulating GlcN-6P. These results suggest that GlcN-6P is a major

co-activator in SiaR-mediated regulation. The regulation of siaP appears to be more complex. Expression of siaP was elevated 30- to 52-fold in strains 2019ΔcyaA ΔnanE, 2019ΔcyaA ΔnanK, 2019ΔcyaA ΔnagB, and 2019ΔcyaA ΔnagA (Figure 3). In contrast, increases of only 2- and 6-fold were observed in 2019ΔcyaA and 2019ΔcyaA ΔnanA, respectively (Figure 3). While SiaR can repress siaP expression [14], transcription of the transporter operon is more directly influenced by CRP. Despite this, siaP expression was not as responsive to cAMP in 2019ΔcyaA and 2019ΔcyaA ΔnanA. These results indicate that in these strains, SiaR is able to exert some control over siaP expression, however the mechanism in which this is accomplished is unclear.

Therein, we have investigated the spacer effect on the microstructures of such organogels and found that various kinds of hydrogen bond interactions among the molecules play an important role in the formation of gels. As a continuous work,

herein, we have designed and synthesized new azobenzene imide derivatives with different substituent groups. In all compounds, the long alkyl chains were symmetrically attached to a benzene ring to form single or three substituent states, with the azobenzene as substituent headgroups. We have found that all compounds could form different organogels in various organic solvents. Characterization of the organogels by scanning electron microscopy (SEM) and atomic force microscopy (AFM) revealed different structures of the aggregates in the gels. We have investigated the effect of alkyl substituent chains and headgroups of azobenzene residues in gelators on the microstructures of such organogels CHIR-99021 in detail and OICR-9429 manufacturer found

different kinds of hydrogen bond interactions between amide groups and conformations of methyl chains. Methods Materials The starting materials, 4-aminoazobenzene and 2-aminoazotoluene were purchased from TCI Development Co., Ltd, Shanghai, China. Other used reagents were all for the analysis purity from either Alfa Aesar (Beijing, China) or Sigma-Aldrich (Shanghai, China) Chemicals. The solvents were obtained from Beijing Chemicals and were distilled before use. Deionized water was used in all cases. 4-Hexadecyloxybenzoic Cell Penetrating Peptide acid and 3,4,5-tris(hexadecyloxy)benzoic

acid were synthesized in our laboratory according to a previous report [28] and confirmed by proton nuclear magnetic resonance (1H NMR). Then, these azobenzene imide derivatives were prepared by simple methods. Simply speaking, different benzoic acid chlorides were synthesized by heating acid compound solutions in sulfoxide chloride and a bit of dimethylformamide (DMF) for about 10 h at 70°C. Then, the prepared benzoic acid chlorides reacted with the corresponding azobenzene amines in dried dichloromethane at the presence of pyridine for 2 days at room temperature. After that, the mixtures were washed with diluted hydrochloric acid and pure water. The organic layer was check details evaporated to dryness. The residues were purified by recrystallization in ethanol solution as a yellow solid. The final products and their abbreviations are shown in Figure 1, which were confirmed by 1H NMR and elemental analysis. Figure 1 Structures and abbreviations of azobenzene imide derivatives with different substituent groups. Gelation test A weighted amount of gelator and a measured volume of selected pure organic solvent were placed into a sealed glass bottle, and the solution was heated in a water bath until the solid was dissolved. Then, the solution was cooled to room temperature in air and the test bottle was inversed to see if a gel was formed.

Full details of the methods are given in Additional File 3. The expression of tight junction-related genes differentially expressed from the microarray analysis was confirmed using qRT-PCR. The expression of seven target genes relative to three reference genes was assessed using the standard curve method. The reference genes (GAPD, SDHA and YWHAZ) were chosen based on the findings see more of Vandesompele et al [52] and their log ratios in the microarray data (close to 1; not differentially expressed). Five target genes (ZO-1, ZO-2,

OCLN, CGN and ACTB) were chosen from the tight junction-related genes that were differentially expressed (all up-regulated) in the microarray analysis. The two other target genes, GJA7 and CLDN3, were chosen to be included because they were down-regulated and not differentially expressed, respectively,

in the microarray analysis. The analysis was carried out as described in Additional File 3 and the data was analysed using Relative Expression Software Tool 2008 (version 2.0.7) with efficiency correction [53]. Fluorescent microscopy Caco-2 cells were grown on Lab Tek II Chamber Slides with Permanox™ coating (Nalge Nunc International Corp, Naperville, IL, USA) for 6 days until confluent. Caco-2 cells were treated with L. plantarum MB452 (OD 600 nm 0.9) or control media for 8 hours (n = 4 per treatment per antibody). After treatment, Caco-2 cells were rinsed twice with selleck inhibitor PBS, fixed in either 4% (w/v) paraformaldehyde for 20 minutes (for CGN and ZO-1) or ice cold 70% ethanol (for ZO-2 and OCLN), quenched with 50 mM NH4Cl (in PBS) for 15 minutes, and blocked with blocking solution (2%

(v/v) foetal bovine serum, 1% sheep serum albumin, 0.1% A-1210477 mouse Triton X-100, 0.05% Tween 20 in PBS, pH 7.2) for 20 minutes. Caco-2 cells were then immuno-stained with the primary antibodies (2.5 µg/mL rabbit Sunitinib mw anti-ZO-1, 1.25 µg/mL rabbit anti-ZO-2, 2.5 µg/mL rabbit anti-occludin, 1 µg/mL rabbit anti-cingulin; Zymed, Invitrogen, NZ) in blocking solution for 1 hour, followed by a PBS wash (0.1% Triton X-100, 0.05% Tween 20 in PBS) to reduce non-specific staining, and the secondary antibody, Alexa Fluor 488 goat anti-rabbit IgG (5 µg/mL for ZO-2, 10 µg/mL for rest; Invitrogen, NZ) in blocking solution for 1 hour. The slides were imaged with a fluorescent microscope (Leica DM2500 microscope, Leica DFC420C camera) with the following settings: exposure 1.1 ms, saturation 2.25, gamma 1.52, gain 8.4× and magnification 40×. The images were viewed using LAS Image Overlay software (Leica Application Suite v1.8.2). Acknowledgements This work was funded by the AgResearch Internal Investment Fund. RCA is funded by a New Zealand Foundation of Research, Science and Technology Postdoctoral Fellowship (AGRX0602). The authors acknowledge the contribution of Kelly Armstrong (fluorescent microscopy) and Paul Maclean (gene ontology and KEGG pathway analysis).

Error bars indicate one positive and one negative standard deviation calculated as described in the methods. Categories increasing in representation at wider taxonomical ranges are hued blue. Categories www.selleckchem.com/products/MDV3100.html decreasing in representation at wider taxonomical ranges are hued red. Other categories are hued green. Phylogeny of the genus Xanthomonas Our phylogenetic analysis was based on 989 INCB018424 in vivo OG (1,084,777 bp, Additional file 2), which included all markers used in previous Xanthomonas

phylogenetic analyses. Both, the Maximum Likelihood tree and the Bayesian consensus tree reconstructed the same well-supported topology, with bootstrap supports of 100% for all the nodes (out of 1,001 replicates). The same relationships were also obtained with Maximum Parsimony (bootstrap support

of 100% with 1,000 replicates). A total of four clades were obtained in the phylogenomic reconstruction. The first clade includes X. oryzae, the second comprises X. vasicola, the third one groups together X. fuscans, X. euvesicatoria and X. axonopodis, and the fourth clade contains X. campestris (Figure 2a). These results agree with previous phylogenies of the genus [11, 17, 35, 42]. In order to further advance on the knowledge of the ancestral relationships of the genus Xanthomonas, and in this website particular the species Xylella fastidiosa, we performed a new analysis including three additional genomes in the Xanthomonadaceae family: Xylella fastidiosa str. 9a5c (GenBank entry AE003849.1), also a plant pathogen, but strictly transmitted by insect vectors; Pseudoxanthomonas suwonensis str. 11-1 (GenBank entry CP002446.1), a bacterium isolated from environmental samples but more commonly found in contaminated ones; and Stenotrophomonas maltophilia str. R551-3 (GenBank entry NC_011071.1), a common soil colonizer which has also been reported as a human opportunistic pathogen. These species are hereafter termed Xyf9, Pxs1 and StmR, respectively.

This new analysis was based on a collection of 228 genes automatically compiled by the Unus library using Bit Score Ration (BSR). The resulting phylogeny revealed that the genus Xanthomonas is not monophyletic, with Xylella fastidiosa as its sister clade. X. albilineans should be placed in an independent genus in order for the taxonomy to match the phylogeny of the group (Figure 2b), as previously see more noted [42]. This result differs from that presented by Pieretti and collaborators, based on seven housekeeping genes [42], where X. albilineans and X. fastidiosa form a single clade ancestral to all other Xanthomonas. Figure 2 Genome-based phylogeny of Xanthomonas. Consensus phylogenetic tree of strains of (a) Xanthomonas based on the 989 OGs, with X. albilineans as an outgroup and (b) Xanthomonas and some genomes from the close relatives Pseudoxanthomonas, Xylella and Stenotrophomonas based on 228 identified using the BSR automated method.