In this investigation, the isolate S halophilum strain LY20 was

In this investigation, the isolate S. halophilum strain LY20 was selected for further study because it appeared to be the best selleck screening library producer of extracellular amylase and protease. To date, there are no reports for amylase and protease production at the same time from one isolate, because the protease can hydrolyze other proteins such as amylase. However, maximal production of both enzymes was observed simultaneously during the stationary growth

phase of LY20 (Fig. 2). This particular phenomenon could be explained that the amylase was not the substrate of the protease, which was confirmed by SDS-PAGE after incubating the two enzyme solutions (80 °C and pH 10.0) for 30 min (data not shown). There are many reports on isolation of amylases from halophiles (Mellado et al., 2004; Litchfield, 2011), but pure preparation of halophilic β-amylase has not been obtained. In this study, purification of an β-amylase from LY20 was reported. Similar enzyme was previously described from Halobacillus sp. LY9 (Li

& Yu, 2011), but its enzymatic properties were mostly obtained from crude extracts. Molecular weight of the β-amylase was determined to be 81 kDa (Fig. 3, lane 2). selleck chemicals The value was higher than other β-amylases from nonhalophiles (Shen et al., 1988; Young et al., 2001). The enzyme showed an optimal activity at 70 °C and excellent thermostability under high temperatures. These characteristics made it obviously different from other β-amylases, which were neither

active nor stable at temperatures above 65 °C (Shen et al., 1988; Young et al., 2001). It is desirable that amylases check details should be active at high temperature for gelanization (100–110 °C), liquefaction (80–90 °C), and saccharification (60–65 °C) for the application in the starch industry. Until today, amylases from bacteria belonging to genus Bacillus are heavily used in the starch-processing industry (Mamo & Gessesse, 1999; Demirkan et al., 2005). As thermostability is an important feature for amylolytic enzymes, the β-amylase from LY20 might be industrially exploited for starch liquefaction and saccharification. Molecular weight of the purified protease was estimated to be 30 kDa on SDS-PAGE. Similar values presented other halophilic proteases previously characterized (Karbalaei-Heidari et al., 2007a, b; Xiong et al., 2007). The enzyme showed the optimal activity at 80 °C. In contrast to other proteases from halophiles (Amoozegar et al., 2007; Karbalaei-Heidari et al., 2009), it required relatively higher temperature to maintain the maximum activity. Moreover, high thermostability over a wide temperature range (30–80 °C) was observed. These properties made it potential use in industrial applications that require high temperatures. The amylase and protease from LY20 were found to be highly active and stable in the presence of higher concentrations of NaCl.

Studies in N europaea have

Studies in N. europaea have VX-770 molecular weight linked the expression of nirK and norB genes with the reduction of nitrite to nitrous oxide via nitric oxide (Beaumont et al., 2002, 2004b; Schmidt et al., 2004). Similarly, the ability of Nitrosospira spp. to produce nitrous oxide has been suggested to involve orthologous genes (Shaw et al., 2006; Garbeva et al., 2007), although a direct linkage between this activity and nirK or norB expression has not yet been demonstrated in any Nitrosospira spp. The

present study showed no effect of nitrite on the expression of either nirK (Fig. 2) or norB (data not shown) in N. multiformis, which is understandable at the molecular level as neither gene has a recognizable nitrite-responsive regulatory protein-binding motif in its promoter region (Norton et al., 2008). The more surprising result was the lack of increased nirK mRNA levels in N. eutropha from exposure to nitrite (Fig. 2) as

the ncgABC-nirK operon, promoter-proximal NsrR-binding motif, and NsrR repressor share high sequence identity between N. europaea and N. eutropha (Cantera & Stein, 2007a; Stein et al., 2007). Together, the data suggest that while the expression of the NirK enzyme is vital to nitrite reduction (Schmidt et al., 2004) and tolerance (Beaumont et al., 2005; Cantera & Stein, 2007b) in N. europaea, it may play a lesser role in N. eutropha and N. multiformis or is constitutively expressed to perform these Sodium butyrate functions. mRNA levels of the three remaining genes, norB, cytL (encoding cytochrome P460), and cytS (encoding cytochrome c′-β) were not affected by nitrite in any of the AOB, suggesting find more constitutive expression in the presence of this toxic metabolite (data not shown). In N. europaea, it was suggested that norB is constitutively expressed during aerobic metabolism (Beaumont et al., 2004b), but is induced during anaerobic metabolism (Beyer et al., 2009) and during growth in the presence

of NaNO2 (Yu & Chandran, 2010). We were unable to confirm induction of norB expression by NaNO2, but did indicate a constant presence of norB mRNA (i.e. 0.03–0.08% of the 16S rRNA gene pool) for all three AOB in all incubations. Although the present study examined only a small subset of shared genetic inventory among three AOB strains, the data revealed that the regulation of these genes was not predictable based on sequence or regulatory motif similarities. This observation was particularly surprising for the nirK genes of the two Nitrosomonas strains. Thus, nitrite and probably other metabolites of AOB are certain to have physiological and genetic effects that vary from strain to strain. This variability must be recognized when building predictive models of how environmental factors, like transiently high nitrite loads, affect AOB physiology, gene expression, and nitrification rates.

Miller, Bronx-Lebanon Hospital Center, New York City, New York, U

Miller, Bronx-Lebanon Hospital Center, New York City, New York, USA; Robert Kass, Travellers Medical and Vaccination Centres of Australia, Adelaide, Australia (December

1997 to March 2001 only); Patrick Doyle and Wayne Ghesquiere, Vancouver General Hospital, Vancouver, British Columbia, Canada; Elizabeth D. Barnett, Boston University, Boston, Massachusetts, USA; Paul Holtom, Jeff Goad, and Anne Anglim, University of Southern California, Los Angeles, California, USA; Nancy Piper Jenks and Christine Kerr, Hudson River Health Care, Peekskill, New York, USA; and Jose Flores-Figueroa and Pablo C. Okhuysen, Travel Medicine Research Clinic, Cuernavaca, Morelos, Mexico. buy Buparlisib
“In travel medicine, as in other specialties, independent prescribing of medication has traditionally been the domain of practitioners like physicians, dentists, and midwives. However, a 2011 ruling in the Netherlands expands independent Selleck FK228 prescribing and introduces

supplementary prescribing by nurses, with expected implementation over the next few years. As specialist nurses will not be eligible for independent prescribing, this study addresses supplementary prescribing, specifically by travel health nurses. Such nurses will work in partnership with an independent prescriber, usually a physician. After the physician evaluates a patient’s condition and needs, the nurse may prescribe from an open or limited formulary. This supplementary approach seems appropriate in travel medicine, which is highly protocolized. A questionnaire survey was conducted to assess whether travel health nurses themselves aspire and feel competent to prescribe, and what training they might need. All travel health nurses in the

Netherlands received a questionnaire seeking their anonymous response. The ZD1839 manufacturer response rate was 58%. Self-reported compliance with protocols and quality criteria was high; 82% of respondents aspire to prescribe and 77% feel competent to prescribe. Of the latter, 22% indicated that ongoing access to a doctor would remain important, and 14% preferred to prescribe under certain conditions like a restricted number of medicines. The reason most frequently given for not feeling competent was the need for additional education before obtaining prescribing rights (40%). Aspiration to prescribe was the only significant predictor for feeling competent to prescribe (odds ratios: 6.8; 95% confidence intervals: 3.5–13).

These agents block more proximally in the signaling cascade, whic

These agents block more proximally in the signaling cascade, which may explain their clinical success. In contrast, p38 MAPK may be too distal in the signaling pathway to be a relevant target.[19] The JAKs were initially discovered in the 1990s. The JAK family of tyrosine kinases consists of four members, JAK1, JAK2, JAK3 and tyrosine kinase-2 (TYK2). Although JAKs were initially coined ‘just another kinase’ due to their uncertain function, these molecules are now known to play a central role in cytokine signaling[20]

when coupled with STAT molecules. The JAK/STAT pathway is responsible for signal transduction of the type I and type II cytokine receptor family, which act as receptors of interferons, interleukins and colony-stimulating factors. Erythropoietin, thrombopoeitin, growth hormone, prolactin and leptin also associate with these receptors and rely on JAK PF01367338 signaling.[21] Upon receptor ligation, a single JAK or combination of JAKs selectively associate

with the receptor’s cytoplasmic domain, leading to phosphorylation and activation of STATs. STATs are DNA binding proteins that, once phosphorylated, dimerize and translocate PD0325901 into the nucleus where they regulate transcription of STAT-dependent genes.[20] JAK1 and JAK3 are mostly aligned with inflammation activation, whereas JAK2 plays a large role in hematopoiesis (Table 1).[22] TYK2 is associated with immune response and may play a role in allergic inflammation.[23] Interestingly, JAK3 associates with the common gamma chain-containing receptor that shares IL-2, IL-4, IL-7, IL-9, IL-15 and IL-21 as ligands. In the mid-1990s it was shown that mutations in JAK3 lead

to severe combined immune deficiency (SCID) due to failure of signaling of the aforementioned cytokines and the subsequent failure of development of functional B, T and natural killer (NK) cells.[24] This discovery provided great insight into the potential role of JAKs as immunomodulators (Table 2). As shown through recent drug development and clinical trials, JAK inhibition is now poised to expand the treatment options for RA. Defective erythropoiesis Defective myelopoiesis Anemia Neutropenia Immunodeficiency 17-DMAG (Alvespimycin) HCl Increased allergy Defective Th1 differentiation Defective interferon signaling Tofacitinib is a small-molecule selective inhibitor of JAK1, JAK3 and to a lesser extent JAK2. Tofacitinib is the first kinase inhibitor to be approved for use in the United States for the treatment of moderately to severely active RA. However, in July 2013, the European Medicines Agency voted not to approve tofacitinib for use in RA. This decision stemmed largely from concerns that there was not a consistent enough reduction in disease activity and structural damage to outweigh the risks of serious infection, malignancy and laboratory abnormalities. Table 3 summarizes the phase 2 and phase 3 clinical trials of tofacitinib.

This easily spread pathogen could change the epidemiology of TD i

This easily spread pathogen could change the epidemiology of TD in Nepal.29–32 The data from the current study were gathered in 2001 to 2003, so the situation may have further evolved since this study was performed. Although 77% of cases with diarrhea presented in the first week of illness, no significant difference Acalabrutinib was noted in the percentage of bacterial pathogens found with diarrhea lasting greater than 1 week versus less than 1 week (Table 4).

Protozoan pathogens namely Giardia and Cyclospora were significantly more likely to cause diarrhea lasting longer than 1 week (Table 4). Cyclospora remained a significant and highly seasonal pathogen in Nepal. Its impact on tourists is less, mainly because the disease peaks during the monsoon season when fewer tourists visit Nepal.33,34 The rate of diagnosis of Giardia (around 10%) is unchanged from previous studies. The low rates of Entamoeba histolytica and Cryptosporidium have also remained unchanged.3,5 Helminths, as in our previous studies, are rarely found in the stools of patients with acute diarrhea, and none were detected in this study population. Multiple pathogens

were once again found to be common. Because click here pathogens were found in 27% of asymptomatic controls, it is likely that not all the pathogens present in a patient with diarrhea are causing symptoms. However, it does reinforce that in a highly endemic environment, if self-treatment of TD is not successful in eradicating

symptoms, other etiologies mainly parasitic may have to be sought. Despite the slight drop in ETEC numbers that may be biased by inclusion of patients with prior FQ treatment, ETEC remains an important pathogen causing 15% of diarrhea with an identifiable etiology (Table 2). Cholera B toxin subunit vaccines, shown to produce significant protection against ETEC strains producing LT and LT, Edoxaban ST combined,35 may be effective in preventing 10% of diarrhea in Nepal considering 70% of strains from cases in this study expressed LT or LT and ST enterotoxins. Better ETEC protection could be expected from newer vaccine candidates that employ both LT toxoid along with fimbrial antigens in our environment where 91% isolates from cases were either LT enterotoxin or CFA positive or both. Use of currently available cholera B toxin subunit vaccine for travel to Nepal with less than 10% of diarrhea prevention cannot be strongly recommended. This update on the microbiology of TD in Nepal should help travel medicine practitioners deliver pretravel advice regarding treatment of TD in Nepal. Besides following the usual food and water precautions, travelers should carry an FQ and azithromycin in their medical kit. For empiric self-treatment, one of the antibiotics should be used first with the other one reserved for treatment failures. For returned travelers with diarrhea lasting longer than 1 week, parasitic as well as bacterial etiologies should be sought.

To investigate surfactant production by R leguminosarum swarm ce

To investigate surfactant production by R. leguminosarum swarm cells, a drop-collapsing test was conducted following the method described by Jain et al. (1991). Briefly, swarm cells were grown in the swarm medium and then a suspension of cells from the edge of a swarming population was prepared find more 7 days and 3 weeks after inoculation. A 10 μL cell suspension (OD600 nmc. 2.0) was spotted on the surface of the hydrophobic lid of a plastic Petri dish. The cell suspension drop was observed for

spreading, which would indicate the presence of surfactants. Distilled water and 0.2% sodium dodecyl sulfate were used as negative and positive controls, respectively. Transmission electron microscopy was click here performed by slightly modifying the procedure used by Miller et al. (2007). The R. leguminosarum strains were grown on solid (1.3% agar) TY plates (for vegetative cells) and on swarm plates (for swarmer

cells). A suspension of the bacteria from the plate cultures was prepared using sterile double-distilled water. For the swarm plates, cultures were taken from the tip of the swarm front and from the center of the plate. A formvar carbon-coated grid was placed on top of a cell suspension drop for 3 min and excess liquid was removed. To determine the arrangement of the swarmer cells, the grid was placed directly on top of the swarm plate, at the tip of the swarm front. Staining was performed using 1% uranyl acetate for 30 s. Samples were observed using a Hitachi-7650 transmission electron microscope and images were taken using an AMT Image Capture Engine. The expression of flagellar genes in R. leguminosarum VF39SM swarmer cells was compared with the expression in R. leguminosarum vegetative cells. We used pre-existing gusA fusions to flagellin (flaA) and flagellar Wilson disease protein regulatory genes (visN, and rem) (Tambalo et al., 2010). Vegetative cells were grown on a solid swarm medium (1.3% Bacto agar) for 8 days at room temperature and in swarm broth medium for 48 h. Swarmer cells were grown in swarm

plates for 2 weeks at 22 °C. Broth cultures were directly used for a β-glucuronidase (gusA) assay, whereas for plate cultures, cells were taken from the edge of a swarming population and vegetative cell population and were suspended in swarm broth. The gusA activity of the fusions was measured as described by Jefferson et al. (1986) and modified by Yost et al. (2004). All data given are the means of triplicate experiments. The antibiotic resistance patterns of vegetative and swarmer cells of R. leguminosarum were determined by growing the cells in swarm medium using 1.3% (solid plate) and 0.7% (swarm plate) Bacto agar. Antibiotic solutions were added onto sterile paper discs and then dried for 20 min. The antibiotics used were cephalexin (50 μg), nalidixic acid (50 μg), rifampicin (20 μg), and chloramphenicol (30 μg).

Furthermore, Tn5251-like elements are highly capable of capturing

Furthermore, Tn5251-like elements are highly capable of capturing other genetic elements carrying different antibiotic resistance determinants such as the mef(E) and erm genes conferring macrolide resistance, aadE, sat4 and aphA-3 conferring resistance to streptomycin, streptothricin and kanamycin, respectively. These features make these elements successful in disseminating multidrug resistance determinants among pathogenic bacterial species. In this context, characterization

of Tn5251 contributes to the understanding of the Alectinib nmr mechanisms of the spread of antibiotic resistance. This study was supported by the European Commission grants ANTIRESDEV HEALTH-F3-2009-241446 and by Universita’ degli Rapamycin Studi di Siena (PAR). “
“In a growth-restricting environment, mutants arise that are able to take over bacterial populations by a process known as adaptive mutation or stationary-phase mutation. This process is best studied in Escherichia coli. The genus Pseudomonas represents one of the largest groups of bacteria able to colonize multiple habitats and to adapt rapidly to new environments. The majority of bacteria including pseudomonads contain a different set of DNA polymerases and DNA repair enzymes

than those identified in E. coli. The aim of this review is to provide an overview of the results of studies of mutagenic processes in pseudomonads and to discuss these results in the light of the mechanisms of stationary-phase mutagenesis discovered in E. coli. Conditions for unrestricted growth are rarely met in natural environments, and therefore, most bacteria are in a state of slow or nongrowth, also called as a stationary phase (Poulsen et Glutathione peroxidase al., 1995; Bååth, 1998). Under stressful, growth-restricting conditions (e.g. nutrient starvation, during colonization of the host organism), microbial populations can rapidly evolve. Genetic changes in microbial populations can occur fast through the acquisition and incorporation of foreign DNA or through mutation. Genetic changes that result from the introduction of mutations

into DNA can arise by various mechanisms, including those caused by DNA damage, and via errors introduced during DNA replication. Replication errors can result from the failure of base selection, proofreading and DNA mismatch repair (MMR), which act sequentially to ensure the fidelity of replication (Schaaper, 1993). Mutagenesis occurring in growth-restricted cells is called adaptive mutation or stationary-phase mutation (Foster, 1999; Rosenberg, 2001). It has been suggested that a variety of environmental stresses induce genomic change in bacteria, generating occasional fitter mutants and potentially accelerating the evolution of bacterial populations (Metzgar & Wills, 2000; Rosenberg, 2001; Tenaillon et al., 2001; Bjedov et al., 2003; Kivisaar, 2003; Miller, 2005; Foster, 2007; Galhardo et al., 2007; Robleto et al., 2007; Baquero, 2009).

The induction of LTD in the IC required activation of the N-methy

The induction of LTD in the IC required activation of the N-methyl-d-aspartate (NMDA) receptor, metabotropic glutamate receptor (mGluR)5, and L-type voltage-gated calcium channel. Protein phosphatase 1/2A and endocannabinoid signaling are also critical for the induction of LTD. In contrast, inhibiting protein kinase C, protein kinase A, protein kinase Mζ or calcium/calmodulin-dependent protein kinase II did not affect LFS-evoked LTD in

the IC. Bath application of the group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine produced another form of LTD in the IC, which was NMDA receptor-independent and could not be occluded by LFS-induced LTD. Our studies have characterised the basic mechanisms of LTD in the IC at the network level, and suggest that two different forms of LTD may co-exist in the same population PLX4032 nmr of IC synapses. “

prototypical effects of the cannabis extract delta9-tetrahydrocannabinol (THC) are characterized by a tetrad of actions, consisting of analgesia, catalepsy, sedation, and hypothermia, all of which are mediated by activation of CB1 receptors. Initial studies of the cellular distribution of CB1 receptors have indicated that they are located primarily on axon terminals of GABAergic interneurons, and their most obvious cellular action is a reduction in transmitter release at these inhibitory synapses. However, the behavioral effects of THC are attenuated by removing CB1 receptors from cortical Palbociclib mouse and striatal projection neurons

(Monory et al., 2007). Collectively, these findings indicate that complex physiological mechanisms mediate the effects of cannabinoids and CB1 receptor stimulation. This complexity is also apparent in the spinal dorsal horn, a CNS area critically involved in the processing Farnesyltransferase of pain signals, as highlighted in the study by Zhang et al. (2010) published in this issue of EJN. Part of the analgesic action of cannabinoids is believed to originate from blockade of excitatory neurotransmission between C-fiber nociceptors and central neurons located in the spinal dorsal horn and trigeminal sensory nucleus (Morisset & Urban, 2001; Liang et al., 2004). Yet, when studied at a cellular level, the most prominent action of CB1 receptor activation again is a reduction in GABAergic and glycinergic inhibition mediated by dorsal horn interneurons (Jennings et al., 2001; Pernia-Andrade et al., 2009). In this issue of EJN, Zhang et al. (2010) used a new approach to quantify the effect of CB1 receptor activation on nociceptive transmission. In slices of rat spinal cord with incoming sensory nerve fibers attached, they electrically stimulated incoming C-fiber nociceptors to evoke neurotransmitter release from these axons.

The melt-curve analysis was performed immediately after the ampli

The melt-curve analysis was performed immediately after the amplification protocol with 0.4 °C increments per 10 s for 85 cycles from 65 to 97 °C. The PCR products were visualized and analyzed using the iQ5 real-time PCR

detection system (Bio-Rad Laboratories). The comparative Ct method (Livak & Schmittgen, 2001; Xu et al., 2010) was used to analyze the relative expression of targeted genes. The untreated cells were cultured anaerobically in TSB (pH 7.3) at 37 °C for 20 h. All experiments were conducted in duplicate for three replicates. Data INCB024360 were analyzed using statisticalanalysissystem software (SAS). The general linear model (GLM) and least significant difference (LSD) procedures were used to determine significant mean differences among strains and culture conditions at P < 0.05. The planktonic and biofilm cell growths of S. aureus KACC13236, S. aureus CCARM 3080, S. Typhimurium KCCM 40253, and S. Typhimurium CCARM 8009 were evaluated in TSB at pH 5.5 and 7.3 under anaerobic conditions (Table 3). At pH 5.5, the planktonic cell growths PD-0332991 manufacturer of antibiotic-susceptible strains S. aureus KACC13236 and S. Typhimurium KCCM 40253 were inhibited during the 48-h incubation, showing a decrease in cell counts to 5.59 and 6.25 log CFU mL−1, respectively. However,

at pH 5.5 the planktonic cells of antibiotic-resistant strains S. aureus CCARM 3080 and S. Typhimurium CCARM 8009 increased to 6.78 and 7.47 log CFU mL−1, respectively Protirelin (Table 3). At pH 7.3, the planktonic cell populations of S. Typhimurium KCCM 40253, and S. Typhimurium CCARM 8009 increased to approximately 9 log CFU mL−1 after 48-h incubation, while the number of planktonic S. aureus KACC13236 cells was reduced by 0.6 log CFU mL−1, compared to the initial number (6.24 log CFU mL−1). The highest biofilm cell numbers were 8.26 and 8.32 log CFU mL−1

for S. aureus CCARM 3080 in TBS at pH 5.5 and pH 7.3 after 48-h cultivation, respectively, while the fewest biofilms were formed by S. Typhimurium KCCM 40253 in TSB at pH 5.5. The MICs of the antibiotics ampicillin, aztreonam, cefotaxime, cefoxitin, ceftazidime, cephalothin, oxacillin, and piperacillin against S. aureus KACC13236, S. aureus CCARM 3080, S. Typhimurium KCCM 40253, and S. Typhimurium CCARM 8009 were determined as shown in Tables 4 and 5. As shown in Table 4, the planktonic and biofilm cells of S. aureus CCARM 3080 were more resistant to most antibiotics than those of S. aureus KACC13236. Compare to S. aureus planktonic cells, the biofilm cells were highly resistant to most antibiotics. The MIC values for ampicillin, cefotaxime, cefoxitin, ceftazidime, oxacillin, and piperacillin were ≥ 256 μg mL−1 against the biofilm cells of S. aureus CCARM grown in TSB at pH 5.5 and 7.3. The planktonic and biofilm cells grown in TSB at pH 5.

Sparkle (Lee & La Rue, 1992) In Trifolium repens roots, ethylene

Sparkle (Lee & La Rue, 1992). In Trifolium repens roots, ethylene inhibits cortical cell division, a process that is indispensable for nodule primordia formation (Goodlass & Smith, 1979). To obviate some of the inhibitory effects of ethylene in nodule formation, development and function, some rhizobial strains utilize different mechanisms for lowering ethylene levels such as the production of the CX-4945 enzyme 1-aminocyclopropane-1-carboxylate (ACC) deaminase; this enzyme is responsible

for the cleavage of ACC (the immediate precursor of ethylene in plants) to ammonia and α-ketobutyrate (Honma & Shimomura, 1978), contributing to increase the competitiveness of the strains because of advantages in the processes of nodule formation and occupancy MK-8669 mw (Ma et al., 2003b, 2004). Other rhizobial strains lower ethylene levels by producing the compound rhizobitoxine, an inhibitor of the plant enzyme ACC synthase (Sugawara et al., 2006). The prevalence of ACC deaminase genes in rhizobia has been studied primarily in Rhizobium spp. (Ma et al., 2003a; Duan et al., 2009). In these studies, many Rhizobium spp. have been found to possess an acdS gene and produce ACC deaminase under free-living conditions. For example, in a rhizobia collection of isolates from Saskatchewan (Canada), 27 Rhizobium isolates possessed an acdS gene and were able to produce

ACC deaminase, thus, showing that acdS genes are present throughout Rhizobium isolates (Duan et al., 2009). On the other hand, notwithstanding reports documenting the presence of ACC deaminase in Mesorhizobium spp., not much is known about the environmental distribution of acdS genes in this bacterial genus. The first report on acdS gene presence in Mesorhizobium was obtained following the complete sequencing of Mesorhizobium sp. MAFF303099 (Kaneko et al., 2000). Subsequently, the presence of an acdS

gene in the symbiosis island of Mesorhizobium loti R7A was also reported (Sullivan et al., 2002). However, when Mesorhizobium sp. MAFF303099 and Mesorhizobium ciceri UPM Ca-7 were tested for ACC deaminase activity and the presence of an acdS gene, no activity was detected and the acdS gene was not found in M. ciceri (Ma et al., 2003b). Recently, the genome sequences of Mesorhizobium (-)-p-Bromotetramisole Oxalate opportunistum WSM2075T (Lucas et al., 2011a), Mesorhizobium australicum WSM2073T (Lucas et al., 2011b), and Mesorhizobium ciceri bv. biserrulae WSM1271 (Lucas et al., 2011c), revealed the presence of an acdS gene in these strains. In some strains of Mesorhizobium, the production of ACC deaminase has been shown to be an important mechanism to promote nodule formation. When compared to the wild-type strain, Mesorhizobium sp. MAFF303099 acdS knockout mutant has a decreased ability to form and occupy nodules, losing both its effectiveness and competitiveness (Uchiumi et al., 2004).