In one of these studies a comparative analysis was Carfilzomib nmr performed between 53 HIV-positive lymphoma patients and a matched cohort (66% non-Hodgkin and 34% Hodgkin lymphoma) of 53 HIV-negative patients [110]. The incidence of relapse, OS and PFS were similar in both cohorts. A higher nonrelapse mortality within the first year after ASCT was observed in the HIV-positive

group (8% vs. 2%), predominantly because of early bacterial infections, although this was not statistically significant and did not influence survival. In the other study performed by the EBMT, the outcome of 68 patients from 20 institutions (median age, 41 years; range, 29–62 years) transplanted after 1999, for relapsed NHL (n = 50) or Hodgkin lymphoma (n = 18) was reported [111]. At the time of ASCT, 16 patients were in

first CR; 44 patients were in second CR and beyond, PR, or chemotherapy-sensitive relapse; and 8 patients had chemotherapy-resistant disease. At a median follow-up of 32 months (range 2–81 months), PFS was 56%. Patients not in CR or with refractory disease at ASCT had a worse PFS (RR: 2.4 and 4.8, respectively) as is frequently reported in the HIV-negative click here setting. Thus, in the HAART era, HIV patients with chemosensitive relapsed ARL should be considered for ASCT according to the same criteria adopted for HIV-lymphoma patients. We recommend that patients deemed fit for intensive chemotherapy should receive a second-line chemotherapy regimen (level of evidence 1C), which may contain platinum (level of evidence 2C). We recommend that those patients responding to second-line chemotherapy (CR or PR) should be considered for HDT with ASCT (level of evidence

Ketotifen 1C). Specific response criteria for NHL in HIV-positive patients have not been described, but the International Working Group response criteria defined for the general population are generally used and are shown in Table 4.8 [21]. Response to treatment is assessed by clinical evaluation, CT scanning and bone marrow biopsy (if the CT scan shows CR and BM was involved at diagnosis). It is usual to assess response half way through treatment, i.e., after 3–4 cycles of R-CHOP chemotherapy or 2 cycles of R-CODOX-M/IVAC. However, the role of 18F-FDG PET scanning during therapy is less clear due to the high false-positive rate [112] and is thus currently not recommended. At the end of treatment, in addition to the mid-treatment investigation, an 18F-FDG PET scan is recommended as in the HIV-negative setting it has been shown to be superior to CT scanning in detecting residual disease with a very high negative predictive value [21]. These investigations should be performed at least 4–6 weeks after the last cycle of chemotherapy and 8–12 weeks after radiotherapy.

Transient GSK458 cost pupil

dilation in humans was elicited after presentation of a visual stimulus in the periphery. The evoked pupil responses were modulated systematically by stimulus contrast, with faster and larger pupil responses triggered by higher contrast stimuli. The pupil response onset latencies for high contrast stimuli were similar to those produced by the light reflex and significantly faster than the darkness reflex, suggesting that the initial component of pupil dilation is probably mediated by inhibition of the parasympathetic pathway. The contrast modulation was pronounced under different levels of baseline pupil size. Together, our results demonstrate visual contrast modulation on the orienting pupil response in humans. “
“The acoustic startle reflex is strongly inhibited by a moderate-intensity acoustic stimulus that precedes the startling stimulus by roughly GDC0449 10–1000 ms (prepulse inhibition, PPI). At long interstimulus intervals (ISIs) of 100–1000 ms, PPI in rats is reduced by the muscarinic receptor antagonist scopolamine. Here, we studied the

role of GABA receptors in PPI at full ISI ranges in both mice and rats. In B6 mice, PPI begins and ends at shorter ISIs (4 and 1000 ms, respectively) than in Wistar rats (8 and 5000 ms). The GABAA antagonist bicuculline (1 mg/kg i.p.) reduced PPI at ISIs near the peak of PPI in both rats and mice. The GABAB antagonist phaclofen (10 or 30 mg/kg i.p. in rats or mice, respectively) reduced PPI only at long ISIs, similar to the effects of the muscarinic antagonist scopolamine (1 mg/kg i.p.). The effects of phaclofen and scopolamine were additive in rats, suggesting independent effects of GABAB and muscarinic receptors. Patch-clamp recordings of startle-mediating PnC (nucleus reticularis pontis caudalis) giant Phosphatidylethanolamine N-methyltransferase neurons in rat slices show that EPSCs evoked by either trigeminal or auditory fiber stimulation were inhibited by

the GABAA/C agonist muscimol or the GABAB agonist baclofen via postsynaptic mechanisms. Hyperpolarization of PnC neurons by muscimol was reversed with bicuculline, indicating that postsynaptic GABAA receptors strongly inhibit PnC giant neurons needed for startle. Therefore, GABA receptors on PnC giant neurons mediate a substantial part of PPI, with GABAA receptors contributing at the peak of PPI, and GABAB receptors adding to muscarinic effects on PPI at long ISIs. “
“The oral part of the pontine reticular formation (PnO) contributes to the regulation of sleep, anesthesia and pain. The role of PnO γ-aminobutyric acid (GABA) in modulating these states remains incompletely understood. The present study used time to loss and time to resumption of righting response (LoRR and RoRR) as surrogate measures of loss and resumption of consciousness.

Usuku et al. [33] followed the changes in drug resistance mutations in Selleck Daporinad a patient receiving HAART. Mutations detected in the plasma were not present or were infrequently present in the proviral DNA.

The discrepancy persisted for more than 3 years. It is important to emphasize that the peripheral blood pool of lymphocytes represents about 2% of the total number of lymphocytes in normal young adult men [34]. Schnuda et al. [35] showed that the small blood lymphocytes recirculate continuously between the peripheral blood and the lymph nodes in the rat, with each cycle having a duration of less than 3 min. In this article, we report the results of a prospective study assessing the prevalence and persistence of HIV-1 drug resistance mutations in proviral DNA from purified CD4 cells compared with those in plasma viral RNA before therapy initiation in treatment-naïve patients. We also evaluated the evolution of HIV-1 drug resistance mutations in proviral DNA before and after therapy initiation, and plasma RNA mutation patterns in patients remaining treatment-naïve. As 95 to 99% of

infected cells are CD4 cells [36], and in order to confirm the utility of resistance testing in provirus, we used direct sequencing of HIV-1 proviral DNA in purified CD4 cells to follow the evolution of drug resistance mutations in treated and untreated patients and compared the findings to those obtained from HIV-1 viral RNA using the ABI 310 Epigenetics inhibitor Prism (Applied Biosystems, Foster City, California). We further chose not to use cloning but

direct population sequencing as this is routinely used in clinical settings. Between May 2002 and July 2007, genotypic resistance Methamphetamine testing was performed on cell-free and cell-associated virus from 69 patients who were not receiving treatment (Table 1). The study was approved by the local ethics committee and informed consent was obtained from each patient. HIV-1 seropositive status was confirmed according to accepted methods. The therapeutic histories of all patients were checked by asking specific questions when they signed the informed consent form and by consulting their clinical records. When documented histories were absent, we contacted the physicians responsible for the patients’ care. This confirmed each patient as HIV drug naïve. Checking the therapeutic histories of all patients can be difficult but is important when studying drug mutations in treatment-naïve patients. Virus was successfully sequenced for 63 of the 69 selected individuals at baseline, both in plasma and in cells. Fifty-eight per cent of the patients were European and 42% non-European, mostly from central Africa. Thirty-nine per cent of the sequenced HIV-1 viruses were subtype B.

The fact that a significant physiological effect was seen when CsrA was overexpressed in a ∆litR strain suggests that the regulatory components upstream of litR are not involved in mediating the observed increase in luminescence. For example, Linsitinib if the V. fischeri system was regulated in a manner similar to V. cholerae through LuxO, then CsrA levels would have had no impact on luminescence output in the ∆litR strain. Instead, CsrA appears

to be regulating luminescence levels at some point in the quorum-sensing pathway downstream of LitR. At high cell density, the upstream quorum-sensing signaling cascade in V. fischeri results in derepression of litR (Fig. 1). LitR in turn not only activates luxR transcription, but also other processes in the cell that are important for host-colonization, motility, and metabolism (Fidopiastis et al., 2002; Studer et al., 2008). Selleck Trametinib In V. cholerae, CsrA is known to indirectly control the activity of LuxO, which in

turn modulates the activity of four Qrr sRNAs and the LitR homologue HapR (Lenz et al., 2005). Interestingly, although the quorum-sensing pathways of V. cholerae and V. fischeri contain some homologous components, the regulation and role of these components has evolved in a different manner. The V. cholerae system has no equivalent of LuxR in its regulatory cascade, and therefore, it could be speculated that it needs to have more sensitive control of expression of its LitR homologue, HapR, through CsrA, LuxO and multiple Qrr sRNAs (Lenz et al., 2005). However, in the V. fischeri system, differential regulation of LitR and LuxR may work together to give the cells the flexibility they need to adapt to changing environmental or metabolic conditions. It was hypothesized that CsrA must in some way cause activation of luxR in a LitR-independent manner. Because LitR is a transcriptional activator of luxR, its disruption leads to lower levels of luxR transcription, and therefore lower levels of luminescence expression, because

Rebamipide the LuxR-AHL complex controls luminescence. The effect of CsrA on the system may be masked in the wild-type strain because of luxR transcription already being highly activated. To determine whether the increase in luminescence observed in PMF8 (pJW3) was because of an increase in luxR transcript levels, quantitative RT-PCR was performed on cDNA samples obtained from ES114 (wild type) and PMF8 (∆litR) strains carrying pJW3 or pJW4 to modulate CsrA levels. In ES114, the luxR transcript level insignificantly decreased with increasing CsrA expression, but in PMF8, the amount of luxR transcript significantly increased as the amount of csrA transcript was increased (Fig. 4a and b). Thus, the impact of CsrA on luminescence described above was manifested by the different dependence of the luxR transcript level on CsrA expression in ES114 vs.

, 2006; Sisto et al., 2009; Fujimoto et al., 2011). Two primer sets have hitherto been reported as L. rhamnosus GG-specific primer sets (Brandt & Alatossava, 2003; Ahlroos & Tynkkynen, 2009). However, few studies have used the strain-specific primer sets, and the qualities

of the sets remain to be characterized. In this study, the two published L. rhamnosus GG-specific primer sets were evaluated by focusing on strain specificities of the sets for future use. All strains used in this study are shown in Table 1. L. rhamnosus GG (=ATCC 53103) was obtained from the American Type Culture Collection and used as positive control. L. rhamnosus DSM 20021T was from the German Collection of Microorganisms and Cell Cultures and buy Ganetespib used as negative control. A number of dairy isolates and human clinical isolates originating from different countries and identified as Epacadostat datasheet L. rhamnosus were obtained from the Belgian Coordinated Collection of Microorganisms/LMG. The strains were cultured

in MRS broth at 37 °C for 20 h. Bacterial DNA was extracted from 1 mL of the cultured cells as previously described (Endo et al., 2007). Two different L. rhamnosus GG strain-specific PCR systems were used in this study, and all PCR primers used are shown in supporting information Table S1. The first PCR system targets a putative transposase gene in L. rhamnosus GG as described by Ahlroos & Tynkkynen (2009). Preparation of the reaction mixture and amplification of DNA

were conducted as described by Ahlroos & Tynkkynen (2009). The second PCR system targets a phage-related gene in L. rhamnosus GG as described by Brandt & Alatossava (2003). Preparation of the reaction mixture and amplification of DNA were according to a method previously described (Brandt & Alatossava, 2003). The amplification products were subjected to gel electrophoresis in 1.0% agarose, followed by ethidium bromide staining. Rep-PCR, RAPD, and ERIC PCR fingerprinting Branched chain aminotransferase were carried out for strain differentiation in L. rhamnosus strains. (GTG)5 primer and a primer set REP1R-I and REP2-I were used for rep-PCR (Table S1). Preparation of the reaction mixture and amplification of DNA were according to the method described by Gevers et al. (2001). For RAPD fingerprinting, six different primers (C0540, 1251, OPA-03, D, E, and F) were used (Table S1). Preparation of the reaction mixture and amplification of DNA were performed as described elsewhere (Endo & Okada, 2006). PCR primers ERIC-1 and ERIC-2 were used for the ERIC PCR (Table S1). Preparation of the reaction mixture and amplification of DNA were by the method of Ventura et al. (2003). The amplification products were subjected to gel electrophoresis in 1.0% agarose, followed by ethidium bromide staining.

418, P = 0.0131 and an area effect: F1,22 = 29.23, P < 0.0001; WT vs. KO in BA: P < 0.05; n = 6 WT, 6 KO). The density of Fos cells in PN-1 KO LA was also reduced but did not reach significance. In addition, a comparison of BA no extinction and extinction groups revealed a significant increase in Fos-immunopositive cell density after extinction learning in WT but not PN-1 KO mice [interaction (genotype × treatment) effect: F1,21 = 12.32, P = 0.0023; BA WT no ext. vs. ext.: P < 0.01; BA KO no ext. vs. ext.: P > 0.05; n = 11 WT, 12 KO]. Our results indicate that the deficient

extinction behavior in PN-1 KO mice is associated with altered neuronal activity in the BA. Fos expression in the ITCs and CEA did not show behavior- or genotype-dependent changes. The average number of Fos-immunopositive cells in the ITCs was one per field, while the density of immunopositive cells in the CEA varied between 28 and 32 cells/mm2. In order to HDAC inhibitor examine longer AZD5363 solubility dmso term changes in synaptic activity and plasticity, we used another marker: αCamKII. Following Ca2+ influx through NMDARs or other calcium sources, αCamKII is activated by binding calmodulin and subsequent autophosphorylation (Fink & Meyer, 2002). As an important

player in downstream signaling, it contributes to NMDAR-dependent synaptic plasticity and has been proposed to serve as a molecular switch for memory processes (Fink & Meyer, 2002; Lisman et al., 2002). Local blockade of αCamKII activity in the BLA impairs fear conditioning (Rodrigues et al., 2004), and increased levels of pαCamKII were found at LA synapses 15 min after fear conditioning (Rodrigues et al., 2004). Importantly, αCamKII and pαCamKII are present in the CEA and in the ITCs (McDonald et al., 2002; Royer & Paré, 2002; Rodrigues

et al., 2004). We used laser microdissection to isolate defined amygdala nuclei and subdivisions aminophylline followed by immunoblot analysis to detect discrete patterns of αCamKII phosphorylation. We chose a 2-h time point after the start of the third behavioral session as this should reflect processes downstream from the initial neuronal activation triggered by CS exposure in all behavioral groups. Using extracted protein from laser-dissected tissue samples from the different behavioral groups of WT and PN-1 KO littermates (for behavioral data for these experiments, see supporting Fig. S1C and D), we analysed the changes in pαCamKII relative to αCamKII protein levels (pαCamKII/αCamKII), as well as αCamKII levels relative to actin. The results were normalized to WT CS-only control values. There were no significant differences between WT and KO αCamKII protein levels relative to actin in any of our experiments (supporting Fig. S2). We then investigated fear conditioning and extinction-induced changes in the pαCamKII/αCamKII ratio in the mITCs and lITCs (Fig. 4).

418, P = 0.0131 and an area effect: F1,22 = 29.23, P < 0.0001; WT vs. KO in BA: P < 0.05; n = 6 WT, 6 KO). The density of Fos cells in PN-1 KO LA was also reduced but did not reach significance. In addition, a comparison of BA no extinction and extinction groups revealed a significant increase in Fos-immunopositive cell density after extinction learning in WT but not PN-1 KO mice [interaction (genotype × treatment) effect: F1,21 = 12.32, P = 0.0023; BA WT no ext. vs. ext.: P < 0.01; BA KO no ext. vs. ext.: P > 0.05; n = 11 WT, 12 KO]. Our results indicate that the deficient

extinction behavior in PN-1 KO mice is associated with altered neuronal activity in the BA. Fos expression in the ITCs and CEA did not show behavior- or genotype-dependent changes. The average number of Fos-immunopositive cells in the ITCs was one per field, while the density of immunopositive cells in the CEA varied between 28 and 32 cells/mm2. In order to DNA Damage inhibitor examine longer SB203580 cost term changes in synaptic activity and plasticity, we used another marker: αCamKII. Following Ca2+ influx through NMDARs or other calcium sources, αCamKII is activated by binding calmodulin and subsequent autophosphorylation (Fink & Meyer, 2002). As an important

player in downstream signaling, it contributes to NMDAR-dependent synaptic plasticity and has been proposed to serve as a molecular switch for memory processes (Fink & Meyer, 2002; Lisman et al., 2002). Local blockade of αCamKII activity in the BLA impairs fear conditioning (Rodrigues et al., 2004), and increased levels of pαCamKII were found at LA synapses 15 min after fear conditioning (Rodrigues et al., 2004). Importantly, αCamKII and pαCamKII are present in the CEA and in the ITCs (McDonald et al., 2002; Royer & Paré, 2002; Rodrigues

et al., 2004). We used laser microdissection to isolate defined amygdala nuclei and subdivisions Miconazole followed by immunoblot analysis to detect discrete patterns of αCamKII phosphorylation. We chose a 2-h time point after the start of the third behavioral session as this should reflect processes downstream from the initial neuronal activation triggered by CS exposure in all behavioral groups. Using extracted protein from laser-dissected tissue samples from the different behavioral groups of WT and PN-1 KO littermates (for behavioral data for these experiments, see supporting Fig. S1C and D), we analysed the changes in pαCamKII relative to αCamKII protein levels (pαCamKII/αCamKII), as well as αCamKII levels relative to actin. The results were normalized to WT CS-only control values. There were no significant differences between WT and KO αCamKII protein levels relative to actin in any of our experiments (supporting Fig. S2). We then investigated fear conditioning and extinction-induced changes in the pαCamKII/αCamKII ratio in the mITCs and lITCs (Fig. 4).

To investigate swarming motility, one colony was transferred to Luria-Bertani (LB)

medium containing 0.25% agar and incubated ON at 37 °C. Positive swarmers showed a halo growth zone of >20 mm. The motility assays were repeated for those strains where no motility phenotype was observed. The static biofilm formation assay was performed as described previously (O’Toole et al., 1999), with minor modifications. MH broth was inoculated with one colony and incubated ON at 37 °C. Cultures were subsequently diluted 1 : 100 in fresh MH broth in polystyrene microtitre trays mTOR inhibitor and incubated ON at 37 °C. Adherent cells were washed once with phosphate buffered saline (PBS), stained by incubation with 0.1% crystal violet for 30 min at 4 °C, and washed three times with PBS. Dye was released from the cells using ethanol:acetone (4 : 1) and shaking at 200 rpm for 30 min at room temperature. Absorbance was measured at 595 nm on a FLUOstar Omega spectrometer (BMG Labtech, Offenburg, Germany). The biofilm data represent the average Sotrastaurin of at least three independent experiments of triplicate wells. Planktonic-growing bacteria were removed and the OD600 nm was determined to ensure strains did not show a growth defect. Adherence of A. baumannii strains to A549 cells (human type 2 pneumocytes) (Giard et al., 1973) and Detroit 562 cells (human nasopharyngeal cells) (Peterson et al., 1968)

was determined essentially as described Nutlin 3 elsewhere (Talbot et al., 1996). Cell lines were grown in Dulbecco’s Modified Eagle medium (Invitrogen, Australia) supplemented with 10% foetal bovine serum (Bovogen, Australia). Prior to use, the cell monolayer was examined microscopically to ensure >95% coverage. Washed A549 or Detroit monolayers, in 24-well tissue culture plates, were subsequently infected with a bacterial inoculum containing ~1 × 107 colony forming units (CFU). The inoculum numbers were subsequently determined by viable count assays. After incubation at 37 °C for 4 h, culture medium was removed, and

the monolayers washed three times with 1 mL of PBS. The cell monolayers were detached from the plate by treatment with 100 μL of 0.25% trypsin and 0.02% EDTA in PBS. Eukaryotic cells were subsequently lysed by the addition of 400 μL 0.025% Triton X-100, and serial 10-fold dilutions thereof were plated on LB agar to determine the number of CFU of adherent bacteria per well. The collated data for the adherence assay were obtained from at least three independent experiments and represent the data points for each experiment of quadruplicate wells. All statistical comparisons were based on the Student’s t-test (two-tailed). A total of 52 randomly selected Australian clinical Acinetobacter strains were used in this study of which 50 were A. baumannii isolates, one Acinetobacter gen. sp. 13TU (WM98b) and one Acinetobacter gen. sp. 3 (WM97b). Four non-Australian A.

Woo et al. (2003) observed that tRNA genes in Penicillium mitochondrial genomes this website rarely encoded an intron, with the exception that one 15-bp intron was predicted in tRNA-Pro in P. marneffei; in P. digitatum, all mitochondrial tRNA genes were intron-free. In Penicillium and Aspergillus species, two distinct, 20-tRNA genes containing similar tRNA gene clusters were found that were flanked by cox3, rnl and cox1. It was interesting that the similarity of tRNA gene clusters was not associated with their phylogenetic relatedness, e.g. tRNA-His was located in the tRNA cluster flanked by rnl and cox1 in A. niger, A. tubingensis and P. marneffei,

but was located between cox1 and atp9 in P. digitatum (Fig. 2), showing the close relationship between

Aspergillus and Penicillium mitochondria and indicating that recombination events have occurred in P. digitatum. Both small subunit (rns) and large subunit rRNA (rnl) were identified in the P. digitatum mitochondrial genome, with a length of 1398 and 3592 bp, respectively. Selleckchem HDAC inhibitor The rns gene showed 98% and 86% identity to that in P. chrysogenum and P. marneffei, respectively. The rnl gene contained one group I intron with a length of 1670 bp, which encoded the protein RPS5. The same structure of rnl was also found in the mitochondrial genomes of P. chrysogenum and P. marneffei, as well as in Aspergillus species. This work was supported by the National Natural Foundation of Science of China (30571236 and 31071649) and the earmarked fund for

the Modern Agro-industry Technology Research System (MATRS). “
“Alkylating agents are widespread in the environment and also occur endogenously. They can be cytotoxic or mutagenic to the cells introducing alkylated bases to DNA or RNA. All organisms have evolved multiple DNA repair mechanisms to counteract the effects of DNA alkylation: the most cytotoxic lesion, N3-methyladenine (3meA), is excised by AlkA glycosylase initiating base excision repair (BER); toxic N1-methyladenine (1meA) and N3-methylcytosine (3meC), induced in DNA and RNA, are removed by AlkB dioxygenase; and mutagenic and cytotoxic O6-methylguanine (O6meG) is repaired by Ada methyltransferase. In Escherichia coli, Ada response involves the expression of four genes, ada, alkA, alkB, and aidB, encoding respective proteins Ada, AlkA, AlkB, Adenosine triphosphate and AidB. The Ada response is conserved among many bacterial species; however, it can be organized differently, with diverse substrate specificity of the particular proteins. Here, an overview of the organization of the Ada regulon and function of individual proteins is presented. We put special effort into the characterization of AlkB dioxygenases, their substrate specificity, and function in the repair of alkylation lesions in DNA/RNA. “
“Phosphatidylcholine, the major phospholipid in eukaryotes, is found in rhizobia and in many other bacteria interacting with eukaryotic hosts.

Woo et al. (2003) observed that tRNA genes in Penicillium mitochondrial genomes Enzalutamide rarely encoded an intron, with the exception that one 15-bp intron was predicted in tRNA-Pro in P. marneffei; in P. digitatum, all mitochondrial tRNA genes were intron-free. In Penicillium and Aspergillus species, two distinct, 20-tRNA genes containing similar tRNA gene clusters were found that were flanked by cox3, rnl and cox1. It was interesting that the similarity of tRNA gene clusters was not associated with their phylogenetic relatedness, e.g. tRNA-His was located in the tRNA cluster flanked by rnl and cox1 in A. niger, A. tubingensis and P. marneffei,

but was located between cox1 and atp9 in P. digitatum (Fig. 2), showing the close relationship between

Aspergillus and Penicillium mitochondria and indicating that recombination events have occurred in P. digitatum. Both small subunit (rns) and large subunit rRNA (rnl) were identified in the P. digitatum mitochondrial genome, with a length of 1398 and 3592 bp, respectively. PD0325901 The rns gene showed 98% and 86% identity to that in P. chrysogenum and P. marneffei, respectively. The rnl gene contained one group I intron with a length of 1670 bp, which encoded the protein RPS5. The same structure of rnl was also found in the mitochondrial genomes of P. chrysogenum and P. marneffei, as well as in Aspergillus species. This work was supported by the National Natural Foundation of Science of China (30571236 and 31071649) and the earmarked fund for

the Modern Agro-industry Technology Research System (MATRS). “
“Alkylating agents are widespread in the environment and also occur endogenously. They can be cytotoxic or mutagenic to the cells introducing alkylated bases to DNA or RNA. All organisms have evolved multiple DNA repair mechanisms to counteract the effects of DNA alkylation: the most cytotoxic lesion, N3-methyladenine (3meA), is excised by AlkA glycosylase initiating base excision repair (BER); toxic N1-methyladenine (1meA) and N3-methylcytosine (3meC), induced in DNA and RNA, are removed by AlkB dioxygenase; and mutagenic and cytotoxic O6-methylguanine (O6meG) is repaired by Ada methyltransferase. In Escherichia coli, Ada response involves the expression of four genes, ada, alkA, alkB, and aidB, encoding respective proteins Ada, AlkA, AlkB, aminophylline and AidB. The Ada response is conserved among many bacterial species; however, it can be organized differently, with diverse substrate specificity of the particular proteins. Here, an overview of the organization of the Ada regulon and function of individual proteins is presented. We put special effort into the characterization of AlkB dioxygenases, their substrate specificity, and function in the repair of alkylation lesions in DNA/RNA. “
“Phosphatidylcholine, the major phospholipid in eukaryotes, is found in rhizobia and in many other bacteria interacting with eukaryotic hosts.