The setB gene is transcribed from a promoter which lies more than

The setB gene is transcribed from a promoter which lies more than 1.5 kb upstream of the setB gene (Behrens et al., 2002). According

to our data, the ardD gene promoter is also located distantly this website from the ardD gene in the region of the mer operon, at a distance of more than 3 kbp. We suggest that other non-conjugative transposons may also contain genes that encode products that can inhibit the restriction endonucleases, thereby efficient overcoming restriction barriers. Note that the tniA gene is usually present in integrons and composite transposons conferring antibiotic resistance and is widely distributed among environmental and clinical bacteria. As an example, the transposon Tn6006 contains a nucleotide sequence identical to ardD in the tniA gene. The Tn6006 transposon MG-132 molecular weight belongs to the group of recombinant transposons containing integrons (Fluit & Schmitz, 1999; Labbate et al., 2008).

This study used equipment of centre of collective use of GosNIIgenetika. It was supported in part by the Russian Foundation for Basic Research (grant 10-04-00541), the Federal Program ‘Scientific and pedagogical innovation resources in Russia, 2009–2013’ (Contract P1070 from 4 June 2010) and The Ministry of Education and Science (Contract 16.522.11.7029). “
“Bacteriocins are the toxic proteins produced by bacteria under stress condition to inhibit the growth of closely related bacterial strain(s). In our earlier study, purified recombinant xenocin–immunity protein complex from Xenorhabdus nematophila showed detrimental effect on six different insect gut residing bacteria. In this study, endogenous toxicity assay with xcinA and its catalytic domain under tightly regulated ara promoter was performed. Multiple sequence alignment and homology modelling revealed six conserved amino acid residues in the catalytic domain of xenocin. Site-directed Resminostat mutagenesis was performed in all the conserved residues, followed growth profile analysis of all the mutants by endogenous toxicity assay. Among the six different conserved sites in catalytic domain of xenocin, we have identified one position where mutation resulted

in no measurable reduction in the endogenous toxicity (K564), three positions with measurable reduction in the endogenous toxicity (E542, H551 and R570) and two positions where mutation caused a significant reduction in the toxicity (D535 and H538). Endogenous toxicity assay is validated by in vitro RNA degradation assay. Structural integrity of purified recombinant proteins was confirmed through circular dichroism and fluorescence spectroscopy. Our results indicate that D535 and H538 act as the acid–base pair for RNA hydrolysis. Bacteriocins are ribosomally encoded, structurally, functionally and ecologically diverse toxins produced by bacteria to inhibit the growth of closely related bacterial strain(s) (Riley & Wertz, 2002; Gordon et al., 2007).

The setB gene is transcribed from a promoter which lies more than

The setB gene is transcribed from a promoter which lies more than 1.5 kb upstream of the setB gene (Behrens et al., 2002). According

to our data, the ardD gene promoter is also located distantly selleck products from the ardD gene in the region of the mer operon, at a distance of more than 3 kbp. We suggest that other non-conjugative transposons may also contain genes that encode products that can inhibit the restriction endonucleases, thereby efficient overcoming restriction barriers. Note that the tniA gene is usually present in integrons and composite transposons conferring antibiotic resistance and is widely distributed among environmental and clinical bacteria. As an example, the transposon Tn6006 contains a nucleotide sequence identical to ardD in the tniA gene. The Tn6006 transposon VX-809 ic50 belongs to the group of recombinant transposons containing integrons (Fluit & Schmitz, 1999; Labbate et al., 2008).

This study used equipment of centre of collective use of GosNIIgenetika. It was supported in part by the Russian Foundation for Basic Research (grant 10-04-00541), the Federal Program ‘Scientific and pedagogical innovation resources in Russia, 2009–2013’ (Contract P1070 from 4 June 2010) and The Ministry of Education and Science (Contract 16.522.11.7029). “
“Bacteriocins are the toxic proteins produced by bacteria under stress condition to inhibit the growth of closely related bacterial strain(s). In our earlier study, purified recombinant xenocin–immunity protein complex from Xenorhabdus nematophila showed detrimental effect on six different insect gut residing bacteria. In this study, endogenous toxicity assay with xcinA and its catalytic domain under tightly regulated ara promoter was performed. Multiple sequence alignment and homology modelling revealed six conserved amino acid residues in the catalytic domain of xenocin. Site-directed FER mutagenesis was performed in all the conserved residues, followed growth profile analysis of all the mutants by endogenous toxicity assay. Among the six different conserved sites in catalytic domain of xenocin, we have identified one position where mutation resulted

in no measurable reduction in the endogenous toxicity (K564), three positions with measurable reduction in the endogenous toxicity (E542, H551 and R570) and two positions where mutation caused a significant reduction in the toxicity (D535 and H538). Endogenous toxicity assay is validated by in vitro RNA degradation assay. Structural integrity of purified recombinant proteins was confirmed through circular dichroism and fluorescence spectroscopy. Our results indicate that D535 and H538 act as the acid–base pair for RNA hydrolysis. Bacteriocins are ribosomally encoded, structurally, functionally and ecologically diverse toxins produced by bacteria to inhibit the growth of closely related bacterial strain(s) (Riley & Wertz, 2002; Gordon et al., 2007).

To construct pKS43

and pKS44, the 22-kbp SacI–BamHI-dige

To construct pKS43

and pKS44, the 2.2-kbp SacI–BamHI-digested ermF–ermAM fragments from pKS1 were ligated to the SacI–BamHI sites of pKS41 and pKS42, respectively. pKS40, pKS43, and pKS44 were linearized and used to construct P. gingivalis mutants 83K8, 83K25, and 83K26, respectively, by Napabucasin clinical trial electroporation (Saiki & Konishi, 2007). The introduced mutations of 83K8, 83K25, and 83K26 were confirmed by determining the nucleotide sequences of the DNA regions that were PCR amplified using chromosomal DNA as templates. Porphyromonas gingivalis cells were grown to the stationary phase in BHIHM medium. Before P. gingivalis cell cultures were used in experiments, the turbidity was adjusted to an OD600 nm of 1.0 using a SmartSpec Plus spectrophotometer (Bio-Rad, Hercules, CA). Porphyromonas gingivalis culture was centrifuged at 10 000 g Cetuximab chemical structure for 5 min at 4 °C, and the supernatant was collected (the extracellular fraction). The extracellular fractions (6 mL) were ultracentrifuged at 250 000 g for 90 min at 4 °C. The supernatant was used as the high-speed supernatant (HSS) fraction, while the pellets were suspended

in 0.1 mL of 8 M urea containing 0.5% SDS and used as the high-speed pellet (HSP) fraction. For immunoblot analysis, a 6-mL portion of the extracellular fraction or the HSS fraction was concentrated to 0.1 mL on ultrafiltration membranes (10 000 molecular weight cutoff: Sartorius Stedim Biotech, Göettingen, Germany), diluted with 8 M urea (3 mL), concentrated to 0.1 mL, and subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis Tideglusib (SDS-PAGE). The harvested cells were washed with phosphate-buffered saline (PBS: 137 mM NaCl, 2.7 mM KCl, 4.3 mM Na2HPO4, and 1.4 mM KH2PO4) and sonicated (Ultrasonic generator US-150 with tip #7; Nihonseiki, Japan) to generate the cell extract

fraction. The cell extract fractions were ultracentrifuged at 104 000 g for 30 min at 4 °C and the supernatant was collected (the cytoplasmic/periplasmic fraction). Membrane pellets were resuspended in PBS, solubilized with 2% Triton X-100 for 30 min at 4 °C, and centrifuged (104 000 g for 30 min at 4 °C). The supernatant was collected (the inner membrane fraction), while the pellets were resuspended in PBS and collected (the outer membrane fraction). Subcellular fractions that would not be used in the evaluation of the enzyme activity were prepared with the same buffers supplemented with a protease inhibitor cocktail (1%; Sigma-Aldrich, St. Louis, MO) and N-α-p-tosyl-l-lysine chloromethylketone hydrochloride (0.1 mM; Sigma-Aldrich). Rgp activity was determined in Tris-HCl (100 mM, pH 8.0)-CaCl2 (10 mM)-l-cysteine (10 mM) using 0.4 mM N-α-benzoyl-dl-Arg 4-nitroanilide (Sigma-Aldrich). Kgp activity was determined in sodium phosphate (20 mM, pH 7.5)-l-cysteine (5 mM) using 0.2 mM N-p-tosyl-Gly-Pro-Lys 4-nitroanilide (Sigma-Aldrich). DPPIV, DPP-7, and PTP-A activities were determined in 20 mM potassium phosphate (pH 7.

The interaction was labile to oxidants, such as diamide

The interaction was labile to oxidants, such as diamide PLX-4720 cell line and menadione. Based on these data, NCgl0899 was named spiA (stress protein interacting with WhcA). Physical association and dissociation of the purified His6–WhcA and GST–SpiA fusion proteins, as assayed by in vitro pull-down experiments, were consistent with in vivo results. These data indicated that the

interaction between WhcA and SpiA is not only specific but also modulated by the redox status of the cell and the functionality of the WhcA protein is probably modulated by the SpiA protein. Corynebacterium glutamicum is a Gram-positive bacteria that belongs to the order Actinomycetales, which also includes the genera Mycobacterium and Streptomyces (Ventura et al., 2007). Corynebacterium glutamicum is a remarkable organism and is capable of producing a variety of amino acids and nucleotides in large quantities (Leuchtenberger et al., 2005). Because of the industrial importance of this organism, its relevant genetic and biochemical features have been extensively characterized. Accordingly, strategies that C. glutamicum cells adopt in response to cellular stresses have attracted scientific interests in recent years. WhiB-like genes are a class of genes that perform diverse cellular processes, such as cell division, differentiation, pathogenesis, starvation survival, and stress

response (Gomez, 2000; Steyn et al., 2002; buy Selumetinib Kim et al., 2005; Geiman et al., 2006; Raghunand & Bishai, 2006; Singh et al., 2007; Choi et al., 2009). The whiB gene, which was originally identified and characterized in Streptomyces coelicolor, is a developmental regulatory gene that is essential for the sporulation of aerial hyphae (Davis & Chater, 1992). The whiB homologues are only found in the order Actinomycetales. Seven whiB homologues have been identified in the Mycobacterium tuberculosis

genome and at least six are present in S. coelicolor (Soliveri et al., 2000), whereas only four are found in C. glutamicum (Kim et al., 2005). The WhiB-like Alectinib proteins have four conserved cysteine residues that bind to a redox-sensitive Fe–S cluster (Jakimowicz et al., 2005; Alam et al., 2007; Singh et al., 2007; Crack et al., 2009; Smith et al., 2010), which plays a critical role in controlling protein function. In general, the cluster loss reaction followed by oxidation of the coordinating cysteine thiols that form disulfide bridges is important for activity. For example, S. coelicolor WhiD loses its Fe–S cluster upon exposure to oxygen (O2) and the apo-WhiD may play important roles in cell physiology (Crack et al., 2009). Some WhiB-like proteins may function as transcription factors, as suggested by the presence of predicted helix–turn–helix DNA-binding motif. Recently, the M. tuberculosis WhiB1 protein in its apo-form was shown to have DNA-binding activity (Smith et al., 2010).

Other forms oftreatment, such as surgical excision, may be consid

Other forms oftreatment, such as surgical excision, may be considered by anal cancer multidisciplinary teams (MDTs), but surgery is usually reserved for salvage. There are still some areas of uncertainty about optimum treatment, and eligible

patients should buy STA-9090 be encouraged to participate in trials. Management of relapse: All patients with suspected or confirmed relapse should be discussed by the anal cancer MDT. Those with confirmed loco-regional recurrence should undergo cross-sectional imaging and all treatment options, including surgery, should be considered by the MDT. Palliative radiotherapy, chemotherapy and palliative care should be discussed with patients who have metastatic disease or who are not sufficiently fit to undergo potentially curative treatment. PF-562271 The incidence of anal cancer in people living with HIV is up to 40 times higher compared with the general

population [3] and it occurs at a much younger age [4–7]. The highest risk is in HIV-positive men who have sex with men (MSM) who have an incidence of 70–100 per 100 000 person years (PY) compared with 35 per 100 000 PY in HIV-negative MSM [8]. Recent studies confirmed the high incidence in HIV-positive MSM, other HIV-positive men and in HIV-positive women [9,10]. Importantly, the incidence of anal cancer appears to have risen with the widespread use of HAART [7,9,11–17] and this may relate to the longer survival of people living Masitinib (AB1010) with HIV allowing time for the progression from HPV infection through the phases of anal dysplasia to invasive anal cancer. It is believed that the pathogenesis of invasive anal cancer resembles that of cervical cancer with human papilloma virus

(HPV) infection leading to anal intraepithelial neoplasia (AIN) and ensuing progression from low- to high-grade dysplasia and subsequently, invasive cancer [4,18–20]. This pathogenetic model suggests a role for anal screening by a combination of cytology and high-resolution anoscopy followed by local ablative therapy of AIN. However, as noted in the 2008 BHIVA, BASHH and FFPRHC guidelines, the role of anal screening is not yet proven [1,20,21]. Whilst some centres have instituted screening pilots [22,23], the cost-effectiveness analyses have produced both positive and negative results [24–29]. The presentation of anal cancer can vary from rectal bleeding and anal pain to features of incontinence if the anal sphincters are affected, with some patients being asymptomatic [4]. Many comparative series have shown that people living with HIV who develop anal cancer are younger than HIV-negative individuals with anal cancer [5,30–36]. However, most comparisons suggest that there is no difference in tumour stage at presentation [5,30–39].

The correct diagnosis was

proposed at the first rank by t

The correct diagnosis was

proposed at the first rank by the travel physicians in 70% of the cases, and by KABISA TRAVEL in 72% (p = 0.56), and was cited in the top five ranking of both “competitors” in 88% of the cases (p = 0.85). No significant difference between the performances of travel physicians and of KABISA TRAVEL was observed for any specific diagnosis. Of note, tropical conditions were more frequently correctly diagnosed Pembrolizumab supplier both by travel physicians and by KABISA TRAVEL than the cosmopolitan diseases as first diagnosis (78% vs 56%, p = 0.001 and 83% vs 53%, p < 0.001, respectively) and within the top five ranking (92% vs 82%, p = 0.03, for both comparisons). These differences disappeared when the malaria cases were removed from analysis, except for KABISA TRAVEL for the first diagnosis (75% vs 53%, p = 0.013). Eleven diagnoses were not included in the five first proposals of travel physicians neither in those of KABISA see more TRAVEL; 13 were included by KABISA TRAVEL but not by travel physicians, and 14 were included by travel physicians but not by KABISA TRAVEL. Reasons for missed diagnoses by KABISA (14) were absence of findings (2) or diseases

(1) in the database, not updated incidence (3), wrong computation (2), and atypical clinical presentation (9). When both clinicians and KABISA did not include the correct diagnosis in the first five (11), for KABISA atypical

presentation was the only and constant cause. For missed diagnoses by clinicians alone no data are available in this study. Details on missed diagnoses are provided in Table 3. Finally, when analyzing the subset of 36 patients with final nonconfirmed diagnoses, it is interesting to note that the initial diagnoses proposed by travel physicians and by KABISA TRAVEL were rather similar and often close to this final clinical suspicion (Table 4). The answers to the survey about the clinical utility of KABISA TRAVEL are reported in Table 5. Data were available for 198 patients. Travel physicians reported that they had been influenced by KABISA TRAVEL for the choice of further pheromone investigations in 16% of the cases, but much more frequently when they did not initially find the correct diagnosis (48% vs 12%, p < 0.001). They reported to have been helped for finding the correct diagnosis in 24% of the cases, and also more often when the correct diagnosis had not been mentioned in the initial list (48% vs 21%; p = 0.005). A median of 10 findings was spontaneously entered by the coinvestigators for all cases under study. After the travel physicians had entered all data they found relevant, KABISA TRAVEL still requested additional information in 81.5% of the cases. A median of three additional findings was asked by the system before considering the cases as fully explored.

[4] Acute pulmonary histoplasmosis (APH) in returning travelers t

[4] Acute pulmonary histoplasmosis (APH) in returning travelers typically presents as a flu-like illness

with high-grade fever, chills, headache, nonproductive cough, pleuritic chest pain, and fatigue.[2] Chest radiographs often show diffuse reticulonodular infiltrates and mediastinal lymphadenopathy. Symptom onset is usually 1–3 weeks following exposure and most individuals recover spontaneously within 3 weeks.[2] Disseminated disease is a rare complication, more likely to occur in persons with severely impaired cellular immunity. The diagnosis of APH in returning travelers is usually made by serology.[2] Complement fixation and immunodiffusion are the most widely used PCI-32765 research buy methods. Serology tests peak approximately 4–6 weeks after the onset of infection and are typically negative in the first month, thus it is important to obtain paired acute and convalescent samples.[3] The sensitivity for acute pneumonia with Decitabine diffuse infiltrates is 40%–80%.[3] Serological tests are less useful in immunosuppressed patients, of whom up to 40% do not mount a measurable antibody response.[3] Antibodies may persist for several years after acute infection and low false-positive complement fixation titers are attributed to previous asymptomatic infection in endemic areas.[3] Histoplasma polysaccharide antigen can be detected

in urine, serum, cerebrospinal fluid, or bronchoalveolar lavage fluid, but antigen tests are not available in all countries. The diagnostic yield is highest when both urine and serum are tested.[5] In a recent evaluation

of 130 patients with APH, antigen detection was 82.8% in the subset in whom both urine and serum were tested.[5] As with serological tests, cross-reactivity can occur with other endemic mycoses such as blastomycosis and coccidioidomycosis.[4] Culture (on Sabouraud’s dextrose agar) provides the strongest evidence for diagnosis but requires invasive sampling and has low sensitivity in mild disease.[3, 4] Typical histopathological appearances in biopsied lung are caseating granulomas and characteristic budding yeast forms.[3] The Infectious Diseases Society of America has developed guidelines for the treatment of histoplasmosis.[6] Antifungal treatment is not usually indicated for mild to moderate APH in immunocompetent persons. For patients who continue to have symptoms Rebamipide for >1 month, itraconazole is recommended.[6] Patients with moderately severe to severe APH should receive liposomal amphotericin B followed by itraconazole.[6] Methylprednisolone is advised during the first 1–2 weeks if there are respiratory complications, including hypoxemia or significant respiratory distress.[6] Patients with disseminated disease and those with underlying immunosuppression should receive a longer duration of therapy.[2, 6] Outbreaks of histoplasmosis have been increasingly reported in association with travel to endemic areas.

Cells were grown in Balch medium III at 35 °C with shaking (Balch

Cells were grown in Balch medium III at 35 °C with shaking (Balch et al., 1979; Kalmokoff et al., 1988). An inframe deletion mutant in flaK derived from M. maripaludis Mm900 was described previously (Ng et al., 2009). These cells are nonflagellated, but piliated and complementation of flaK in trans restores flagellation. Using the flaK mutant as a starting host, the subsequent deletion of the prepilin peptidase eppA was accomplished using the technique of Moore & Leigh (2005). An approximately 1-kb region upstream

of eppA was amplified using the primers P1: 5′-CGCGGATCCCATTTCTATCAATTTTCCAC and P2: 5′-TTGGCGCGCCGGGGAATTATTCGCTCTTTGATAT. Primers P3: 5′-TTGGCGCGCCGGCGTTATAAATTATCTGGTGGGA and P4: 5′-CGCGGATCCCGTTTGACTGTTTGAACAGC Kinase Inhibitor Library were used to amplify approximately 1 kb downstream of the gene. Both P2 and P3 primers had AscI sites incorporated into them (underlined in primer), allowing for Selleckchem CH5424802 AscI cleavage of the two PCR products, followed by ligation and PCR amplification with primers P1 and P4 to generate an approximately 2-kb fragment that contained an inframe deletion version of eppA. Using the BamHI sites

incorporated into primers P1 and P4 (underlined), this piece was cloned into pCRPrtNeo and transformed into the existing M. maripaludis flaK deletion strain with transformants screened for the eppA deletion by PCR using primers P5: 5′-CTGGAGCTGTATGAAATGCAACTGG and P6: 5′-CCTGCATTATCCCAGGTCATCC, which amplify across the deleted region. Similarly, the same plasmid was transformed into the Mm900 strain and transformants screened for the check eppA deletion leading to mutants that were wild type for flaK, but deleted only for eppA. Wild-type and mutants cells were grown for 18 h at 35 °C before ethanol-sterilized substrates to be tested for attachment were added. Incubation continued at 35 °C with gentle agitation for a further 24 h. Tested substrates

included various grids [200 or 400 mesh uncoated gold, nickel (Agar Scientific, Essex, UK) and molybdenum grids (Gilder Grids, Grantham, UK)], mica, silicon wafer chips (Agar Scientific) and glass. To examine whether surface contact influenced the production of pili, the flaK deletion mutant was grown on Balch medium III plates (with 1.5% w/v Noble agar) for 4 days. Colonies were removed, resuspended in medium and briefly centrifuged. The pellet was gently resuspended in 2% glutaraldehyde in 100 mM sodium phosphate buffer, pH 7.2–7.4, containing 2% w/v NaCl for 30 min and examined by transmission electron microscopy (TEM), as described below. Wild-type and mutant cells were examined by TEM to identify the presence of surface appendages. Cells were fixed with 2% glutaraldehyde in 100 mM sodium phosphate buffer, pH 7.2–7.

A much higher HIV prevalence was observed in 2008, reaching 49% (

A much higher HIV prevalence was observed in 2008, reaching 49% (95% CI 44–56%) in women delivering at the Manhiça Hospital. Table 1 shows the prevalence by age group for each time-point. Age-specific prevalence showed an upward trend up to 35 years of age, with a peak in women aged 25–29 years, although small sample sizes for older age groups limit conclusions on age-specific prevalence. HIV incidence was estimated at the mid-point between prevalence surveys using two estimation methods and the three epidemic scenarios (described in the Methods section). The incidence results across

all age groups were similar for all four estimation strategies. The highest incidence was observed in younger age groups up to 35 years (results not shown). The overall incidence, after weighting for age group population size, increased over

time (Fig. 1). As shown in the table inset into Figure 1, an increase was observed after 2001, when the incidence was Tanespimycin price approximately 3.5 per 100 person-years, rising to 14 per 100 person-years MAPK inhibitor in 2004, and to over 20 per 100 person-years between 2004 and 2005. In Figure 1, the time regression curve adjusted to the incidence estimation shows an increase in HIV incidence up to 2005, with apparent stabilization thereafter. After omitting one by one each point prevalence in the sensitivity analysis, no significant differences were observed between estimations (results not shown), suggesting consistency of the model. When the upper and lower limits of the incidence rate estimation were calculated for 95% bootstrapping Carnitine palmitoyltransferase II CIs, no significant differences in the limits of the estimations

were observed between the methods (shown only for method 2 in Fig. 1). The results of this analysis show that the prevalence of HIV infection among women of reproductive age in Manhiça, Mozambique has increased significantly in under 10 years. HIV prevalence in this population rose from 12% in 1999 to 49% in 2008. This could be attributable to a sustained increase in HIV incidence or to decreased mortality in HIV-infected individuals. The current results show a significant increase in HIV incidence from 1999 to 2005, and then a plateau from 2005 onwards, despite a steadily increasing prevalence until 2008. These results suggest that the HIV epidemic is in a mature phase in Mozambique. It is important to mention that the two methodologies used to estimate the incidence were in agreement, thus suggesting consistency of the findings [1]. cART was introduced in the Manhiça District Hospital in 2005. It is possible that the introduction and expansion of cART since 2005 might have contributed to a decrease in HIV-related mortality in adults. High cART coverage leads to lower mortality in HIV-infected individuals, thus apparently increasing HIV prevalence despite a stable HIV incidence. However, cART coverage is likely to be low in Manhiça, as has been observed for Mozambique as a whole (24% coverage in 2007) [8].

marthii and L rocourtiae,

marthii and L. rocourtiae, LY2157299 order for further evaluating and supplementing this assay. Furthermore, this approach has the potential to contribute to a more comprehensive taxonomy

platform for the Listeria genus and is suitable for use in epidemiological research and classification of bacteria. Grant numbers and sources of support: this work was supported by Science Foundation for The Excellent Youth Scholars of Health Bureau of Zhejiang Province (2008QN007). The authors wish it to be known that, in their opinion, the authors D.J. and Y.L. should be regarded as the joint first authors. “
“Phenyl lactic acid (PLA) has been widely reported as a new natural antimicrobial compound. In this study, 120 Lactobacillus plantarum strains were demonstrated to produce PLA using high-performance liquid chromatography.

Lactobacillus plantarum IMAU10124 was screened with a PLA yield of 0.229 g L−1. Compared with all previous reports, this is the highest PLA-producing lactic acid bacteria (LAB) when grown in MRS broth without any optimizing conditions. When 3.0 g L−1 phenyl pyruvic acid (PPA) was added to the medium as substrate, PLA production reached 2.90 g L−1, with the highest 96.05% conversion rate. A lowest PLA-yielding L. plantarum IMAU40105 (0.043 g L−1) was also screened. It was shown that the conversion from PPA to PLA by lactic dehydrogenase (LDH) is the key factor check details in the improvement of PLA production by LAB. Comparing the LDH gene of two strains, four amino acid mutation sites were found in this study in the LDH of L. plantarum IMAU10124. “
“Mycoplasma mycoides subsp. mycoides (Mmm) strain Afadé had previously been shown to undergo spontaneous phase variations between an opaque capsulated variant and a translucent (TR) variant devoid of a capsule but able to secrete cell-free exopolysaccharides. This phase variation is associated with an ON/OFF genetic switch in a glucose permease gene. In this study, in vivo and in vitro assays were conducted to compare the virulence of the two variants and their abilities to resist host defence. Capsulated variants

were shown, in a mouse model, to induce longer bacteraemia that was correlated with better serum resistance in vitro. In contrast, TR variants displayed better ability to adhere to an inert support, linked to the absence of a capsule, Phenylethanolamine N-methyltransferase changes in cell surface hydrophobicity and increased resistance to antimicrobial peptide and hydrogen peroxide. The switch from one variant population to another, which was observed both in vivo and in vitro under stress conditions, is further discussed as a means for Mmm to modulate its interactions with animal hosts during different stages of the disease. “
“RodZ (YfgA) is a membrane protein well conserved among bacterial species and important in the determination of cell shape and motility, although the molecular mechanism involved is not well established.