Screening of subjects took place between 21 and 3 days 4SC-202 mouse before first study drug administration. Enrolled subjects were randomized to treatment sequences A/B or B/A. Treatment A consisted of almorexant 200 mg once daily on day 1–10 and a single dose of 25 mg warfarin co-administered on day 5; treatment B consisted of a single dose of 25 mg warfarin on day 1. A 2-week washout period between learn more treatments was respected. A dose of 200 mg almorexant was chosen because it was expected to be well tolerated

and it was the highest dose investigated in phase III trials. Study drugs were administered in the morning to subjects in the fasted state, with breakfast served 2 h thereafter. During both treatments, subjects were confined to the study

center from approximately 12 h prior to warfarin administration until 144 h thereafter. Because of the sleep-promoting properties of almorexant, subjects stayed in the clinic under supervision for approximately 5 h after its intake on days 1–4 of treatment A. After this 5-h observation period, a physician determined whether the subject was fully alert and could be allowed to go home or whether there were any residual effects that could be attributed to a sleep-promoting drug (e.g., muscular weakness, dizziness, fatigue, or somnolence). Subjects were not to drive a car or engage in activities that required operating vehicles check details or dangerous machinery. From screening until the end-of-study examination, which was performed 144 h after warfarin administration in the second treatment period, subjects had to refrain from excessive physical exercise and strenuous sports activities and were not allowed to consume cranberries, grapefruit, cranberry juice, or grapefruit juice. Although no effect of grapefruit juice on the pharmacodynamics

of warfarin could be shown [17], cranberry juice increased the international normalized ratio (INR) [18]. This study was conducted in full conformity with the Declaration of Helsinki and its amendments. The protocol was approved by an independent ethics committee (Ethics Committee of the Medical University, Graz, Austria). Each subject provided written informed consent Tacrolimus (FK506) prior to any study procedure. 2.2 Inclusion and Exclusion Criteria Eligible subjects were healthy males aged between 18 and 45 years who had a body mass index between 18 and 28 kg/m2 at screening. Subjects were judged to be healthy based on medical history, physical examination, ECG, vital signs, and clinical laboratory tests. Subjects were not enrolled if they had a history of hemorrhagic disease, frequent nasal, hemorrhoidal, or gingival bleeding, an activated partial thromboplastin time >40 s, an INR >1.15, a low (<150 × 109) or high (>400 × 109) platelet count, or had been treated with any medication (including over-the-counter and herbal medicines) within 2 weeks prior to screening. 2.

Results of RT-PCR and Western blot showed specific MACC1-shRNAs could effectively knockdown expression of MACC1 in OVCAR-3 cells. We also successfully obtained OVCAR-3 cell line with the best inhibitory effects of MACC1 expression for further analysis. As a consequence of MACC1 gene knockdown, the proliferation, migration and invasion of OVCAR-3 cells were obviously inhibited, but the apoptosis rate was significantly increased. These results showed inhibition of MACC1 could suppress the growth and metastatic potential of ovarian carcinoma cells in vitro and in vivo, which suggested MACC1 might implicate in

the growth and metastasis of ovarian carcinoma. MACC1 binds to a 60 bp proximal fragment of endogenous MET promoter, where contains a specific Sp1 binding site which is essential for MACC1-induced activation of MET and subsequent HGF/Met signaling consequences [13]. Once activated, Met CHIR98014 can result in activation of several downstream signaling cascades, such as MAPK and PI3K/Akt pathways [14]. MACC1

protein contains several domains which can participate in MAPK signaling, and MACC1 can be up-regulated by MAPK pathway which has been identified to be essential for HGF-induced scattering [15–17]. In colon cancer cells, MAPK signaling could be hyperactive by transfection of MACC1, and HGF-induced cell scattering mediated by MACC1 could be click here abrogated by MEK specific inhibitors, whereas not by PI3K specific inhibitors [2]. After inhibition of MACC1 by RNAi in ovarian carcinoma

OVCAR-3 cells, we observed that level of Met protein was down-regulated significantly, as well as expressions of p-MEK1/2 and p-ERK1/2 protein, but expression of p-Akt was uninfluenced. Therefore, we presumed that inhibition of MACC1 by RNAi might suppress the malignant behavior of ovarian carcinoma cells via HGF/Met and MEK/ERK pathways, at least in part. Furthermore, increased level of cleaved caspase3 and decreased levels of cyclinD1 and MMP2 protein were detected in ovarian carcinoma cells after RNA interference against MACC1, which suggested cyclinD1, caspase3 and MMP2 should be associated with MACC1 mediated Pyruvate dehydrogenase downstream signaling. HGF/Met signaling plays an important role in cellular growth, epithelial-mesenchymal transition, angiogenesis, cell motility, invasiveness and metastasis [18]. Deregulated HGF/C-met signaling has been observed in many tumors, including ovarian carcinoma, and been proved to contribute to tumor dissemination and metastasis [19]. MAPK and PI3K/Akt pathways have been demonstrated to implicate in cell survival, anti-apoptosis, invasion, metastasis and angiogenesis of malignancies, including ovarian carcinoma [20–22]. Because of these cascades play key roles in carcinogenesis, some specific antibodies and small molecules to neutralize or block the key regulators of these pathways have been used to inhibit tumor growth and metastasis, which exploit effective intervention www.selleckchem.com/products/pnd-1186-vs-4718.html strategies for malignancies [19, 23, 24].

cholerae epidemic strains usually harbor Integrative Conjugative Elements (ICEs) of the SXT/R391 family [12]. SXT/R391 ICEs are self-transmissible mobile elements, ranging in size from 79 to 108 kb, able to integrate into the host bacterial chromosome and to transfer by conjugation. They are recognized for their important role in bacterial genome plasticity [13] and as vectors of antibiotic resistance and alternative metabolic pathways [12]. The name of the SXT/R391 family originates from elements SXTMO10 and R391, respectively discovered in clinical strains of Vibrio cholerae in India [14] and Providencia

rettgeri in South Africa [15]. The two elements are associated with different multi-resistance profiles: chloramphenicol, streptomycin, sulfamethoxazole, and trimethoprim for SXTMO10, and kanamycin, and mercury for R391 [12]. They share check details a highly conserved genetic backbone this website encoding their integration/excision, conjugative transfer, and regulation, but also contain variable DNA found in five insertion sites of the backbone [12]. Each ICE of the family holds specific genes scattered in the conserved sequence that code for resistance to antibiotics and heavy metals, new toxin/antitoxin systems, restriction/modification systems,

and alternative metabolic pathways [12]. To date more than 50 ICEs have been identified and grouped within the SXT/R391 family, most of them discovered in V. cholerae strains. To date, only a few SXT-related ICEs were identified in Africa, most of them through the characterization of the integrase int SXT . Only ICEVchMoz10 from Mozambique (2004) has been completely sequenced and annotated [12]. This ICE has no close relative Fossariinae in Africa except its

sibling ICEVchBan9 isolated in Bangladesh (1994), suggesting the possible spread of SXT-related ICEs between the two continents in recent times. Although the use of horizontally-transferred elements as genetic markers for strain discrimination might appear risky, we recently showed the existence of an ICE/strain association in epidemic V. cholerae strains circulating in the Indian Subcontinent [16]. The association between ICE and V. cholerae reflects the classification proposed by Chun and colleagues to describe homologous intraspecific groups of V. cholerae based on the whole genome alignment of 23 strains isolated over the past 100 years [17]. In this retrospective study, we analysed V. cholerae O1 clinical strains isolated in Luanda (Angola) in 2006. Angola is an endemic area for cholera and was subjected to two major epidemic events in the past three decades. The first see more outbreak (1987-1993) [18] was followed by a thirteen year remission phase until cholera reemerged in 2006 in one of the most severe epidemic outbreaks of the last decade, counting about 240.000 cases [19]. Here we demonstrate that the V.

Data

analysis Conditional logistic regression analysis was used to estimate the risk of hip/femur GDC-0941 ic50 fracture associated with the use of dopaminergic drugs and were expressed as odds ratios (OR) with corresponding 95% confidence intervals (CI). Adjusted odds ratios (ORadj) for hip/femur fracture were estimated after adjustment for the various confounding variables. Final regression models BIBW2992 molecular weight included all potential confounding factors that changed the natural logarithm of the risk estimate with more LXH254 ic50 than 5%. Stratified analyses within current dopaminergic drug users were performed regarding gender, age category,

type of current dopaminergic drug (dopamine agonist, levodopa-containing drug, or combined use) and concomitant use of anticholinergics, antidepressants, antipsychotics or benzodiazepines. In order to differentiate between onset and offset of the effect of dopaminergic drugs on hip/femur fractures, two separate analyses were performed: (1) the onset was investigated by calculating the risk of hip/femur fractures in relation to continuous duration of dopaminergic drug use within current users; (2) the offset was investigated by calculating the risk of hip/femur fractures in relation to the recency of use of dopaminergic drug treatment within ever users. In both analyses, the dopaminergic drug users were subdivided into 10 subgroups based on deciles of the continuous duration of use (or recency of use). An OR was calculated for each of the subgroups.

Spline regression was then used to smooth these estimates and to visualise Methamphetamine any trends. This method has been advocated as an alternative to categorical analysis [31]. Analyses were performed with SPSS 16.0. Spline regression was performed with SAS 9.1.3. Results We identified 6,763 cases with a fracture of the hip or femur and 26,341 matched controls (Table 1). Almost three-quarters (73%) of the study population was female. The mean duration of follow-up before the index date was 5.8 years for cases and 5.7 years for controls. The median age was 79 years for cases and controls.

Cultures of microorganisms were collected by centrifugation from the broth Sotrastaurin mw cultures, washed three times and finally suspended in phosphate-buffered saline (PBS; pH 7.1). The working dilution of the microorganism suspensions was determined by performing sequential measurements of optical densities of cultures at 600 nm and quantification of viable microorganisms by colony counts. For each strain, the correlation between the OD600 and cfu was established. The microorganism cells suspended in DMEM were used for the adhesion and interference assays. Adherence of L. crispatus L1 to Vk2/E6E7 cells was assayed by a method described previously with slight modifications

[46]. Preliminary experiments using 10:1, 100:1, and 1000:1 multiplicities of infection (MOI) were conducted to determine the optimal bacterial-to-epithelial cell ratio in our adhesion model. These pilot investigations demonstrated a saturation of adhesion of L. crispatus L1 to Vk2/E6E7 cells at a MOI of 10:1. Therefore, for all subsequent adhesion experiments described in this study a MOI of 10:1 was utilized. Interference experiments were performed Ruxolitinib in vitro with C. albicans, a potential vaginal pathogen, that showed a significant capacity to adhere to host cells. The procedures described by Osset et al. [47] were used, with some modifications. For exclusion

tests, 1×107 lactobacilli and vaginal epithelial cells were incubated together for 1 h at 37°C in microaerophilic conditions; afterwards, C. albicans cells were added, and incubation was further continued for 1 h. During competition tests, 1×107 lactobacilli and 1×107 C. albicans were mixed and Vk2/E6E7 cell monolayers then inoculated and incubated for 1 h at 37°C in microaerophilic selleck chemical conditions. For displacement tests, 1×107 C. albicans and epithelial cells were incubated together for 1 h at 37°C in microaerophilic conditions. Successively, 1×107 lactobacilli were added and incubation was prolonged for 1 h. Vk2/E6E7 cells were scored for the presence and number of bacteria and C. albicans

attached, and cell observation was performed as indicated above. For exopolysaccharide-interference experiments, Liothyronine Sodium Vk2/E6E7 cell monolayers were treated with EPS as follows: for competition tests, exopolysaccharide (0.01-0.1-1.0 mg∙ml−1) and 1×107 C. albicans were mixed and, successively, Vk2/E6E7 cell monolayers were inoculated and incubated for 1 h at 37°C in microaerophilic conditions. For exclusion tests, vaginal epithelial cells were pre-treated with EPS (0.01-0.1-1.0 mg∙ml−1), before addition of the C. albicans suspension for 1 h at 37°C in microaerophilic conditions. At the concentrations used, the EPS did not affect epithelial cell viability. In preliminary experiments monolayers were pre-treated with EPS for 1, 4, 6 and 18 h at 37°C in microaerophilic conditions. Microorganism adhesion to Vk2/E6E7 cells was assessed by microscopy (×100) after Gram’s stain by counting the number of micro-organisms attached to 30 consecutive cells.

The initial denaturation step was performed for 4 minutes at 95°C. Denaturation temperature was 95°C in the 30 cycles of PCR. Each reaction was performed in a total volume of 50 μl with 3 units FastStart Taq DNA polymerase, 200 μM deoxynucleoside triphosphates, 5 μl 10× PCR reaction buffer (without MgCl2) and 2 mM MgCl2 (all from Roche, Switzerland), 1 μM of each primer and 100 ng genomic DNA. Endonucleases AflIII, ApoI, DdeI and MseI (New England Biolabs, MA, USA) were used for

digestion of the PCR product according the manufacturer’s instructions. Antibiotic susceptibilities Etest® strips (AB BIODISK, Solna, Sweden, distributed in Switzerland by bioMérieux) were used to determine the minimal inhibitory concentrations (MIC) for eFT508 mouse the different antibiotics according to current international recommendations (www.​clsi.​org). A sterile cotton swab was soaked in 0.5 McFarland of bacterial culture and then streaked on agar plates (Mueller Hinton with 5% sheep blood). Ten minutes later, the Etest® strips were applied on the agar plates which were then incubated for 24 h and 48 h at 37°C with 5% CO2 atmosphere. Construction of revertant mutant strains Capsule switch mutant strains were generated for both the encapsulated and the nonencapsulated 307.14 wild type variant using a Janus cassette buy ATM Kinase Inhibitor based on the published method [23]. As a first step, a Janus mutant was made from each of the wild type phenotypes.

Next, the Janus mutant (nonencapsulated) derived from the encapsulated wild type was transformed with DNA from the nonencapsulated wild type strain to create the mutant 307.14 cap-. Also, the

Janus mutant derived from the nonencapsulated wild type was transformed with DNA from the encapsulated wildtype strain to create the mutant 307.14 cap+. Wild type and mutant strains used in this study are listed Buspirone HCl in Table 1 and the amplification and sequencing primers are listed in Additional file 1: Table S1. Pneumococcal strain AmiA9 (a kind gift of Regine Hakenbeck, University of Kaiserslautern, Germany) that harbours the genotype rpsL K56T conferring streptomycin resistance [44] served as template for rpsL K56T amplification. PCR products were purified using the GDC-0941 ic50 Wizard® SV Gel and PCR Clean-Up system (Promega, USA). Stocks of competent recipient 307.14 variants were prepared by growing them in brain heart infusion broth (BHI) (Becton Dickinson, USA) supplemented with 5% fetal bovine serum (FBS) (Merck, Germany) to mid-logarithmic phase (optical density (OD600nm) = 0.5–0.8) followed by a 1:20 subculture in tryptic soy broth (TSB) (Becton Dickinson), pH 7 [45] to OD600nm = 0.13. Bacteria were harvested by centrifugation at +4°C and resuspended in TSB, pH 8 + 15% glycerol (Sigma, USA) for storage at -80°C until use. DNA was extracted using the QIAamp® DNA Mini Kit (Qiagen, Germany) following the manufacturer’s instructions.

Figure 1 HIPK2 immunostaining in breast cancer. Streptavidin-biotin immunoperoxidase staining of invasive breast ductal carcinomas displaying (A) nuclear HIPK2

localization, and (B) cytoplasmic Q-VD-Oph mouse HIPK2 localization. Magnification 40X. (kindly provided by Dr. Marcella Mottolese, IFO-IRE, Rome, Italy). HIPK2 is involved in the p53-mediated repression of Galectin-3 (Gal-3), a β-galactoside-specific lectin with anti-apoptotic activity, involved in tumorigenesis and resistance to chemotherapeutic drugs [43]. Intriguingly, though, Gal-3 is highly expressed in well-differentiated thyroid carcinomas (WDTCs) nonetheless the presence of wild-type p53 supposed to negatively regulate Gal-3. This paradoxical behavior may Selleckchem Fosbretabulin be explained by hypothesizing that in WDTC wtp53 protein is inactive. Thus, Real-Time PCR on total RNA extracted from frozen thyroid CP 690550 tissues samples as well as immuonohistochemistry analyses revealed that HIPK2 is indeed downregulated in WDTCs [44]. In particular, genetic loss at HIPK2 locus 7q32-34 was found by loss of heterozigosity (LOH) analysis in thyroid cancer cells stained with Gal-3 and retrieved by Laser Capture Microdissection (LCM) [44]. This study demonstrates

that the loss of HIPK2 expression in WDTC may be responsible for lack of p53 activation, thus explaining the paradoxical co-expression of wild-type p53 with overexpressed Gal-3. Of interest, HIPK2 LOH was also observed in mice. In particular, a screening for genetic alterations in radiation-induced thymic lymphomas demonstrated that Hipk2 is a haploinsufficient tumor suppressor gene in vivo, showing loss of one Hipk2 allele in 30 % of the tumors and increased susceptibility ID-8 of Hipk2+/− mice to radiation-induced thymic lymphoma [45]. This study provides compelling evidence that

Hipk2 functions as major tumor suppressor in response to ionising radiation in vivo. Interestingly, this function appears to be in part independent of p53. An intact p53 is crucial for chemotherapy-induced apoptosis in MYCN-overexpressing neuroblastoma cells. Thus, MYCN sensitizes neuroblastoma cells to apoptosis by upregulation of the HIPK2/p53Ser46 pathway via ATM-dependent DNA damage response (DDR) that activates HIPK2 [46]. HIPK2 is largely expressed in human primary MYCN amplification (MNA) neuroblastoma tissues and its expression is induced by MYCN, whose inactivation inhibits HIPK2 and impairs p53Ser46 phosphorylation and apoptosis [46]. An abnormal HIPK2 function was recently associated to skin carcinogenesis. This study investigated a link between oncogene E6 of genital high-risk human papillomavirus (HPV) and HIPK2.

A, FixLBj PAS domain (pdb code: 1DRM), with the heme colored grey. C, PAS domain of the M. tuberculosis Rv1364c protein (pdb code: 3KC3), showing the fatty acid in the cavity (in grey). E, cavity of PASHm (pdb code: 3BWL) with the Asp side chains (in yellow) pointing to the 1H-indole-3 carbaldehyde ligand (in grey). In PASBvg (F) the corresponding residues find more are Tyr596 and Asn631. We nevertheless tested the possibility that PASBvg harbors a heme co-factor or a related molecule when present in the full-length BvgS protein in B. pertussis by replacing His643 with Ala. In bona fide

heme-PAS domains, replacement of the His residue abolishes heme binding [31]. Because B. pertussis is virulent in aerobic growth conditions, we reasoned that O2 would most likely be a positive signal for BvgS if the PAS domain harbored an O2-sensing heme, and therefore that a substitution abolishing heme binding should inactivate BvgS. The mutation was introduced into the chromosome of the B. pertussis Tohama I derivative BPSME705 by allelic exchange, and the activity of BvgAS was assessed by using a lacZ Cell Cycle inhibitor reporter under the control of the ptx promoter, which is positively controlled by

BvgAS. The mutated JQ-EZ-05 chemical structure strain expressed ß-galactosidase activity at a level similar to that of the strain containing wt BvgS (Figure 4). Interestingly, BvgSHis643Ala was insensitive to sulfate and nicotinate (Figure 4). Other negative modulators [32] also failed to modulate the activity of the recombinant strain, even at much higher concentrations than those that modulate wild type BvgS (not shown). Thus, the His643Ala substitution appears to make BvgS unresponsive to modulation.

Figure 4 β-galactosidase activities of the recombinant strains producing the BvgS variants. The β-galactosidase activities of the ptx: lacZ fusion were measured as a function of increasing concentrations of nicotinate ADP ribosylation factor or MgSO4. The basal (non-modulated) activities of the three variants tested were not significantly different (P > 0.1) from that of wild type (WT) BvgS. The BPSMΔbvgS and BPSMΔbvgA variants had hardly detectable levels of β-galactosidase activities in all conditions, and therefore they were not included in the figure. In each panel, one and two asterisks represent significantly different activities (with P < 0.05 and P < 0.01, respectively) than that of the same non-modulated BvgS variant. The His643Ala substitution was also introduced into the N2C3 recombinant protein, and the N2C3 variant was purified. Similar to all soluble proteins produced in this work, N2C3His643Ala was dimeric (not shown). Using the thermal shift assay its Tm was determined to be 7°C lower than its wt counterpart (Table 1). Altogether, our data do not support the notion that PASBvg has a heme cofactor. However, His643 appears to be required for BvgS response to negative signals, indicating its functional importance. It also contributes to the thermal stability of recombinant PASBvg.

The best fit obtained for our data was for d = 1, consistent with a dominant 1D electronic transport mechanism in our samples. Figure 6 shows a plot of the natural logarithm of G as a function of T −1/2; the experimental data

shows a linear dependence for almost the complete temperature range. By fitting the function in Equation 1, with d = 1, to the average data curve from sample CNTs_(AAO/650°C), a value of T 0  ≈ 4.4 × 103 K is obtained. For samples CNTs-A and Au-CNTs-B, the values of T 0 from the fit of the average data were ≈ 4.4 × 103 K and ≈ 5.0 × 103 K, respectively. These results are in agreement with Wang et al.’s report [52], in which a 1D dependence within the VRH model is found for CNTs prepared using alumina templates. Although the values check details obtained for T 0 are similar in all three samples, the inclusion of gold nanoparticles implies a larger value for T 0. This is consistent with QNZ manufacturer the fact that forming the gold nanoparticles by drop-casting (T 0 ≈ 5.0 × 103 K) produces noticeable modifications to the Idasanutlin concentration tubular structure of the CNTs compared to those generated through dip-coating (T 0 ≈ 4.4 × 103 K). As an example, several locations in which these changes occur have been indicated by arrows in

Figure 1c. Figure 6 indicates that the inclusion of gold nanoparticles by drop-casting modifies the electronic transport below 60 K (see the curve with red open circle markers in Figure 6). In this low temperature range, only sample Au-CNTs-B exhibit the 1D hopping process, while the other two show a residual metallic behavior, inferred from the tendency to display a constant conductance. In the case of sample Au-CNTs-B, the residual metallic PRKACG behavior of the conductance

is almost non-existent and the VRH model can be extended to very low temperatures to account for the observed behavior. This result is consistent with the fact that the walls of the Au-CNT-B tubes are completely distorted by the presence of AuNPs, as detected by TEM (Figure 1c), and causing the suppression of the metallic conduction. Figure 6 Plots of ln( G ) for the samples CNTs_(AAO/650°C), Au-CNTs-A, and Au-CNTs-B as a function of T −1/2 . In addition to the measured data (open symbols), illustrative error bars have been included for each sample. At this point, it is important to note that the transport measurements were performed using interdigitated microelectrodes, implying that conduction occurs through a mesh of CNTs between the electrode fingers (Figure 5c). Consequently, the interconnections between the CNTs need to be included in any model put forward to describe the conductance in this system. To verify this issue, we prepared an additional sample, labeled as CNTs-2900 K. It contains CNTs with a high degree of graphitization. These tubes were synthesized in the same way described in Section 2.

Indeed, the analysis of unigene compositions in ESTs showed that about 88% of unigenes were obtained from between one (singleton) to four ESTs and less than 3.5% of unigenes were assembled from more than 10 ESTs (Fig. 2B). This finding highlights a low quantitative sequencing depth with the Sanger methodology and advocates next-generation sequencing (NGS) methods, such as Illumina, to fulfill in silico quantitative analysis of this work. The GC content of total sequences is about 35%, which is very close to the genomic GC content of Tribolium castaneum (34%), phylogenetically the closest Coleopteran species sequenced

so far [52]. Sequences covered LY333531 cell line around 5.5 Mb against 14 Mb of predicted transcripts in Drosophila. The distribution of unigenes in the different libraries is presented in selleck Selleckchem Ro 61-8048 Figure 2A. More than 60% of the unigenes were provided by the NOR library, showing the importance of normalization for unigene number enrichment. Blast analysis has shown that most of the first hits were from Tribolium castaneum sequences. This result was as expected

and is linked with the relatively high phylogenetic proximity between Tribolium and Sitophilus. Only about 25% of the unigenes had no Blast annotation that corresponded to the UTR part of the cDNA. Following the Blast2go annotation procedure for High Scoring Pair (HSP) coverage of 0%, 3845 unigenes presented at least one GO term (Fig. 2C). After Interproscan prediction and the Annex procedure, 3995 unigenes presented at least one GO term association. Analysis of libraries One of the objects of this study was to unravel the genes involved in host-symbiont interactions Exoribonuclease within the bacteriome. For this purpose, an in silico subtraction was conducted between SO and AO libraries, which evaluates statistical differences in unigenes prevalence in the presence

or absence of the symbiont in the bacteriome tissue. This analysis identified 11 differentially expressed genes (Table 2). The most differentially expressed gene showed the first blastx hit with a cellular Fatty-acid binding protein (FABP), and presented a calycin domain with the Interproscan tool. It is predicted that it would be upregulated in the presence of SPE. However, this first blastx hit presented a relative low e-value (i.e. 6e-05) and the predicted protein of the sequence showed a weak similarity with the fatty-acid protein (32% on 132 predicted amino acids). This finding highlights the need for additional work to clarify the annotation of this gene. As this gene was also reported as being the most highly expressed in the bacteriome of S. zeamais [30], it is referred to as the “Most Expressed Gene in the weevil Bacteriome” (MEGwB). Table 2 List of unigenes presenting statistically different representations in AO and SO libraries.