We used fabXL::gusA fusions to measure the relative expression of

We used fabXL::gusA fusions to measure the relative expression of the fabXL genes in different conditions. The fabXL genes were induced approximately two-fold in TY, or VMM with 1% hydrolyzed casein, compared with the expression in VMM with mannitol (data not shown). The induction of ropB expression in peptide-containing media requires the ChvG/ChvI two-component system (Foreman et al., 2010). We used a chvG mutant in R. leguminosarum VF39SM (we were unable to construct a chvG

mutant in 3841) to determine whether ChvG Bcl-2 inhibitor is involved in regulating the fabXL genes. The putative promoter sequences used to construct the fabXL::gusA transcriptional fusions are identical to those found in VF39SM, and expression of the fusions in VF39SM was similar to the expression in 3841. VF39SM and the chvG mutant carrying the fabXL::gusA fusions were grown on solid VMM with calcium chloride or VMM with tryptone and calcium chloride, as described previously (Foreman selleck chemical et al., 2010). A roughly fourfold induction in fabXL gene expression was observed in wild-type grown in the presence of tryptone. In contrast, there was no induction of the fabXL fusions in the chvG mutant, suggesting that ChvG is a positive regulator of the fabXL genes in R. leguminosarum (Table 4). As well, the fabXL fusions were generally expressed

at a lower level in the chvG mutant than in wild-type (Table 4), suggesting ChvG is also important for gene expression under non-inducing conditions. Given that the ChvG–ChvI two-component system is thought to be a global regulatory system (Chen et al., 2009), it is possible that the nonspecific decrease in transcription of the fabXL genes is an indirect effect resulting from a significantly affected cell physiology. Our results differ from those found for the chvG homolog, bvrS, in Brucella abortus, where there was no change in the transcript abundance for acpXL or lpxXL in a bvrS Depsipeptide order mutant (Manterola et al., 2005). This observation suggests that although

this two component system (TCS) is a highly conserved global regulator, its role in regulation of cell envelope components may have species-specific complexities. In conclusion, our results demonstrate that the fabXL and ropB genes are part of a cell envelope network required to maintain outer membrane stability. These cell envelope components are strongly conserved among the order Rhizobiales; therefore, continued investigation into the mechanisms and proteins controlling the interactions between ropB and the fabXL genes will provide insight into the mechanisms that regulate gene expression during cell envelope development in free-living and host-associated environments. Lastly, the biological significance of the down-regulation of ropB expression following mutation of LPS structural genes remains an intriguing question meriting further investigation. We gratefully acknowledge Dr. R. W. Carlson for supplying us with the acpXL mutant strain, Rlv22, and Dr. K.

We used fabXL::gusA fusions to measure the relative expression of

We used fabXL::gusA fusions to measure the relative expression of the fabXL genes in different conditions. The fabXL genes were induced approximately two-fold in TY, or VMM with 1% hydrolyzed casein, compared with the expression in VMM with mannitol (data not shown). The induction of ropB expression in peptide-containing media requires the ChvG/ChvI two-component system (Foreman et al., 2010). We used a chvG mutant in R. leguminosarum VF39SM (we were unable to construct a chvG

mutant in 3841) to determine whether ChvG AZD9291 order is involved in regulating the fabXL genes. The putative promoter sequences used to construct the fabXL::gusA transcriptional fusions are identical to those found in VF39SM, and expression of the fusions in VF39SM was similar to the expression in 3841. VF39SM and the chvG mutant carrying the fabXL::gusA fusions were grown on solid VMM with calcium chloride or VMM with tryptone and calcium chloride, as described previously (Foreman Everolimus et al., 2010). A roughly fourfold induction in fabXL gene expression was observed in wild-type grown in the presence of tryptone. In contrast, there was no induction of the fabXL fusions in the chvG mutant, suggesting that ChvG is a positive regulator of the fabXL genes in R. leguminosarum (Table 4). As well, the fabXL fusions were generally expressed

at a lower level in the chvG mutant than in wild-type (Table 4), suggesting ChvG is also important for gene expression under non-inducing conditions. Given that the ChvG–ChvI two-component system is thought to be a global regulatory system (Chen et al., 2009), it is possible that the nonspecific decrease in transcription of the fabXL genes is an indirect effect resulting from a significantly affected cell physiology. Our results differ from those found for the chvG homolog, bvrS, in Brucella abortus, where there was no change in the transcript abundance for acpXL or lpxXL in a bvrS Sitaxentan mutant (Manterola et al., 2005). This observation suggests that although

this two component system (TCS) is a highly conserved global regulator, its role in regulation of cell envelope components may have species-specific complexities. In conclusion, our results demonstrate that the fabXL and ropB genes are part of a cell envelope network required to maintain outer membrane stability. These cell envelope components are strongly conserved among the order Rhizobiales; therefore, continued investigation into the mechanisms and proteins controlling the interactions between ropB and the fabXL genes will provide insight into the mechanisms that regulate gene expression during cell envelope development in free-living and host-associated environments. Lastly, the biological significance of the down-regulation of ropB expression following mutation of LPS structural genes remains an intriguing question meriting further investigation. We gratefully acknowledge Dr. R. W. Carlson for supplying us with the acpXL mutant strain, Rlv22, and Dr. K.

Cells were harvested, lysed and the expression of DnrO was detect

Cells were harvested, lysed and the expression of DnrO was detected by DnrO polyclonal antibody (Fig. 4a). The intensity of the band was measured by imagej software. A twofold excess of DnrO expression was observed in culture incubated with DNR compared with control without DNR (Fig. 4b). We could surmise that in the presence of DNR, the DnrO autorepression is alleviated because it cannot bind to its own promoter sequence (site of repression). This resulted in unhindered transcription of DnrO. As autorepression of dnrO and activation of dnrN is a simultaneous event, an increase

in DNR level in the cells would affect both. This led Pifithrin-�� chemical structure us to investigate further the status of dnrN expression in the same scenario. The addition of DNR to a heterologous strain carrying dnrNO genes affected the in vivo expression of dnrO as shown by Western blot (Fig. 4, compare Lanes 1 and 2). As DnrO functions as an activator for dnrN, we analyzed the expression of dnrN in the presence and absence of DNR. This was done by fusion of dnrN to a promoterless EGFP as a single transcript

(pIJ8660/dnrNO). The construct Selleckchem Ibrutinib was integrated to the S. lividans chromosomal attB site. This was accomplished by mobilizing the E. coli plasmid construct by conjugal transfer. The expression of EGFP was studied in the presence and absence of DNR by confocal microscopy. In the presence of DNR (2 ng), EGFP fluorescence was very low, implying that there is a decrease in dnrN expression (compare plates 1 and 2 in Fig. 5). This means that activation of dnrN is precluded because DnrO cannot bind to its activation site in the presence of DNR. This observation, along with results of the Western blot experiment, suggests that the repression/activation role of DnrO is affected by DNR. Regulation of DNR biosynthesis is a three-tier mechanism involving the three regulatory genes dnrO, dnrN and dnrI. Modulation of expression of these genes by DNR can affect biosynthesis. DNR has been shown to bind to a second site that overlaps with the DnrN-binding sequence (activator site) close to dnrI

promoter (Furuya & Hutchinson, 1996). Competitive inhibition of DnrN binding by DNR has been suggested already (Furuya & Hutchinson, 1996). Modulation Guanylate cyclase 2C of three regulatory genes by the intracellular concentration of DNR and two critical intercalations (dnrN-binding site and dnrO-binding site) seem to regulate, as well as fine-tune, DNR biosynthesis. Based on the experiments described here and previously published work, we propose a model for feedback regulation. The model describes the importance of intracellular concentrations of DNR and DnrO in regulating DNR biosynthesis. DNR production in S. peucetius starts after 48 h of growth in liquid culture medium. DnrO being the first activator, its expression is expected at the early growth phase (Otten et al., 2000). Initially, dnrO promoters are active and dnrN promoter is dormant because of insufficient intracellular activator DnrO (Fig. 6a).

This role for IL-17 in angiogenesis is supported by recent findin

This role for IL-17 in angiogenesis is supported by recent findings that local overexpression of IL-17 in C57BL/6 mice leads to arthritis, with increased vascularity along with angiogenesis.[83, 96] IL-17 can also up-regulate the constitutive release of other angiogenic factors from synovial fibroblasts, including keratinocyte growth factor (KGF), hepatocyte growth factor (HGF) and heparin-binding epidermal growth factor (HB-EGF), all of which are involved in the proliferation of endothelial Dinaciclib price cells.[81, 97] Recently, TNF-positive

Th17 cells have been discussed as potential dangerous cells in driving persistent arthritis in patient with early RA.[78] TNF and IL-17 synergistically have also been proposed to induce the alternative

complement pathway proteins C3 and factor B, both of which are up-regulated in RA synovial tissue.[98] In conclusion, these data strongly suggest that Th17 is a key effector cell in driving the acute phase to the chronic form of RA.[89] A large number of cytokines are active in the joints of patients with RA. It is now clear that these cytokines play a fundamental role in the processes that buy Obeticholic Acid cause inflammation, articular destruction and the co-morbidities associated with RA.[99] Two down-stream mechanisms by which the cartilage degradation occurs have been elucidated: the simultaneous inhibition of proteoglycan and collagen synthesis and the catabolism of the extracellular matrix. It is thought that inflammation in the adjacent synovial tissue and fluids evokes changes in the metabolic

activity of chondrocytes.[88] Furthermore, IL-17 appears to play an active role in the induction of cartilage matrix breakdown through the dysregulation of chondrocyte metabolism.[78, 100] In RA, imbalance occurs in the main cytokine system, including IL-1, IL-6, IL-13, IL-15, IL-18, IL-22, IL-33 and TNF. The joint destruction seen in RA is caused not only by this cytokine imbalance, but also by specific Clomifene effects of the Wnt system and osteoprotegerin on osteoclasts, as well as by dysregulation in matrix production responsible for cartilage damage.[101] Although IL-17F has many biologically overlapping effects with IL-17A, IL-17F is less potent, for example, in activating synovial fibroblasts.[102] IL-17F has been shown to have a cartilage destructive potential effect in vitro.[59] In a mouse model, intra-articular injection of IL-17 into the knee joint resulted in joint inflammation and damage. Moreover, it is shown that blocking IL-17/IL-17R signaling could be effective in the control of RA symptoms and in the prevention of joint destruction.[103] Like IL-17A, IL-17F regulates pro-inflammatory gene expression by a very similar but not identical signaling pathway involving IL-17RA and IL-17RC.[104] Furthermore, data from an experimental model of arthritis indicated IL-17 receptor signaling is a critical pathway in turning acute synovitis into a chronic destructive arthritis.

4) The LacZ activity levels of cells recovered between 12 and 48

4). The LacZ activity levels of cells recovered between 12 and 48 h were low, but increased markedly after 4 days, indicating that a certain incubation period was required for the induction. This delayed expression of LacZ activities was not observed by the constitutively lacZ-expressing

strain, 17616cox::lacZ (Nishiyama et al., 2010), which showed similar levels of LacZ activities at 12 h and 14 days after inoculation in the soil (data not shown). To determine whether the andA operon is essential to survive or grow in soil, the 17616ΔandAc was tested for its ability to proliferate and survive in the soil. The 17616ΔandAc and 17616cox::lacZ cells form white and blue colonies, respectively, on X-gal-containing agar plate. The 1 : 1 mixture of the Ixazomib two kinds of cells was inoculated into the soil sample, the cells PLX 4720 were recovered after various intervals, the CFUs of each type of cells g−1 of soil were counted (Fig. 5a), and the proportion of white colonies to the total (i.e. white plus blue) ones was also calculated (Fig. 5b). During the first 15 days, the CFUs of 17616ΔandAc remained at a low level, whereas the CFUs of 17616cox::lacZ increased. In Fig. 5b, the mutant cell ratio declined during the first week and reached a

steady low level, clearly showing that andA is necessary in the soil environment. We also tested two deletion mutants of ATCC 17616, 17616ΔpdyP and 17616Δsdh. Each mutant carried a chromosomal deletion of a genomic locus that was induced in the soil environment (Nishiyama et al., 2010). Although these mutants were originally included to investigate the

role of the deleted genomic locus in the soil, they showed no decreased CFUs and fitness, and they are controls here (as the results for the two mutants are essentially the same, the result for 17616Δsdh is not shown). Our present study clarified that the andAcAdAbAa gene cluster, predicted to encode anthranilate dioxygenase in B. multivorans ATCC 17616, is indeed involved in the catabolism of tryptophan and anthranilate, and that this gene cluster is under the control of two transcriptional regulators, AndR and Fur, in both the laboratory and soil environments. We RANTES also showed that this cluster plays a pivotal role in the proliferation in the soil environment. We showed that the andA operon is regulated by Fur, which is an iron-responsive transcriptional regulator. The anthranilate dioxygenase belongs to a class of dioxygenases, which require a [2Fe-2S] cluster in its active site (Batie et al., 1991), and it is not surprising that the iron-regulatory scheme operates on the andA operon. However, the effects of the iron-chelating agent and the disruption of fur gene on the transcriptional activity of andA operon were not remarkable (only at the level of twofold change) in B.

An interval of at least 1 month was required between the date of

An interval of at least 1 month was required between the date of baseline CMV viraemia analysis mTOR inhibitor and these endpoints. The potential prognostic factors assessed were sociodemographic variables (sex, age, ethnic origin and HIV transmission category), use of any antiretroviral therapy (ART), CD4 cell counts, HIV viraemia and CMV DNA in plasma. The patients were followed from the date of the available plasma sample collection for the baseline CMV PCR to the

date of the last cohort visit before 31 December 2007. The occurrence of CMV end-organ disease or another OD did not result in follow-up being terminated. To determine the incidence and prevalence of CMV end-organ disease in the SHCS, we used data obtained for the whole population of

the cohort since 1996. ART was defined as the use of an antiretroviral drug(s), either as monotherapy or as dual therapy; HAART was defined as the use of three nucleoside reverse transcriptase inhibitors (NRTIs), or two NRTIs with either a protease inhibitor (PI) or a nonnucleoside reverse transcriptase inhibitor (NNRTI), or four antivirals. CMV DNA was measured in plasma collected at a time when the CD4 count was ≤100 cells/μL. We used an automated CMV real-time PCR (Abbot Molecular, Des Plaines, IL, USA) with a threshold of detection of 20 copies/mL. This method is used routinely to monitor CMV infection in our institution and is described in recent publications [14–16]. In 216 samples, the quantity of plasma was insufficient and Enzalutamide mw the plasma had to be diluted (1:4) in order to measure the CMV DNA, which was positive in 67 samples (31%). The initial threshold of detection of 20 copies/mL could not be guaranteed in these samples and we therefore considered 80 copies/mL to be our global threshold in the survival analysis. The evolution of the annual

incidence rate (assessed in person-years) of CMV end-organ disease from 1996 to 2007 was analysed using Poisson regression (with the year as predictor). The exponential of the regression parameter was interpreted as a relative decrease (or increase) of the incidence rate in a given year compared with the previous year [17]. This model allowed for different changes of the incidence rate between Org 27569 the periods 1996–1998 and 1999–2007, because the reduction in incidence was not linear over the whole observation period. The performance of the CMV DNA measurement in predicting the prognosis of CMV end-organ disease, OD and mortality was assessed using time-dependent receiver operating characteristic (ROC) curves. For each ROC curve, the area under the curve (AUC) and the confidence intervals (CIs) were assessed by bootstrap (1000 simulations). The purpose of this method [18] is to evaluate the performance of a marker in predicting the occurrence of an event, which can happen at different points in time. The closer the AUC is to a value of 1, the better the performance of the test. 0.5 represents an uninformative test.

Taking life-long treatment with a high adherence demand may also

Taking life-long treatment with a high adherence demand may also have emotional effects. Some compounds exacerbate mental health symptoms [7], while others may be associated with side effects (e.g. lipodystrophy) with mental health sequelae [8]. Poor mental health or heavy mental health burden is associated with reduced adherence, which in turn is associated with poorer outcome [6-9]. Therefore, incorporating assessment of mental health

into the routine follow-up of patients at all stages is important but is particularly critical at first presentation in order to establish a baseline. It is also important prior to commencement of ART (see 6.2 Monitoring of ART-naïve patients) and in those individuals with suboptimal adherence and/or virological failure, or signs of mental health symptoms (such Epigenetic inhibitor order as depressed mood, heightened anxiety, relationship concerns, memory or functioning concerns). Cognitive symptoms have been noted from the early days of the

epidemic, ranging from mild cognitive symptoms to more severe memory loss, executive functioning difficulties and cognitive impairment [10]. The advent of treatment has clearly reduced the prevalence of severe cognitive disorders [11, 12], while milder forms have continued in a proportion of patients. There is currently much debate about the prevalence, risk factors for, and prognosis of, mild-to-moderate cognitive impairment in persons taking effective ART Selleck CHIR-99021 (full virological suppression). Joint psychological support standards are currently being consulted on and it is anticipated that these will make recommendations about screening [13], although there is not yet consensus about easy-to-administer and effective measurements. The finalized standards will be available late in 2011. Standardized monitoring of psychological wellbeing at baseline, at annual follow-up and at change points (such as treatment initiation and treatment switching) (III). Having good referral mechanisms to psychological services in place and clear criteria for referral (see BHIVA guidelines on psychological support

[13]) (IV). Inclusion of psychological GPX6 consideration in relation to fertility, drug use, treatment change, side effects, adherence, relationships and doctor–patient interaction (IV). There is no high-grade evidence for what is the optimal frequency at which to measure CD4 T cells in well-resourced health environments. We have considered three different scenarios: initial HIV diagnosis; monitoring ART-naïve patients; and CD4 T-cell counts in patients on ART. Recommendations for how often we should be measuring CD4 T-cell counts are mainly based on expert opinion [1-3]. For ART-naïve patients, we used data from a cost-effectiveness analysis using an HIV simulation model incorporating CD4 T-cell count and plasma HIV-1 RNA load as predictors of disease progression [4].

We cannot live in

isolation and none will be winner if su

We cannot live in

isolation and none will be winner if superiority is sought. “
“To retrospectively investigate and compare the effects of tumor necrosis factor alpha inhibitors (TNFi) on hepatic enzymes in ankylosing spondylitis (AS) patients. A retrospective analysis of the records of 94 AS (66 male, 28 female) patients using TNFi was performed. Patients’ clinical data, Bath Ankylosing Spondylitis Disease Activity (BASDAI) scores, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were all examined. Liver function test (LFTs) results of patients before the treatment and 3, 6 and 12 months after treatment with TNFi were investigated. Aspartate transaminase see more (AST) and alanine transaminase (ALT) levels were investigated as indicators of LFTs. The TNFi drugs used Tacrolimus cell line were infliximab (n = 28), adalimumab (n = 32) and etanercept (n = 34). Pre-treatment values of ESR, CRP and BASDAI

scores were 28.3 ± 20.1 mm/h, 1.5 ± 1.2 ng/dL and 5.2 ± 0.8, respectively. Following TNFi use there was a statistically significant decrease in disease activity score (P = 0.001). There was a significant increase in LFT at the third month evaluation compared to the initial values, while the average value was within normal range (baseline AST 19.6 ± 10.8 U/L, ALT 19.1 ± 6.4 U/L, third month AST 31.3 ± 21.6 U/L, ALT 28.1 ± 18.1 U/L, P = 0.001). Drug group comparison analysis revealed a significant difference in the adalimumab group value at the end of the first year, but no other significant difference in the data for the other months (P > 0.05). No significant correlation was determined between initial disease activity scores and LFT. TNFi use-associated

rises in hepatic enzymes were determined compared to pre-treatment but the mean values Acetophenone remained within normal limits. Considering the cases in the literature, in daily practice patients must be carefully monitored for liver function before treatment and at follow-up. “
“To determine the prevalence of sexual dysfunction (FSD) among women with rheumatoid arthritis attending the Rheumatology Clinic in Universiti Kebangsaan Malaysia Medical Centre (UKMMC) and Hospital Putrajaya, Malaysia, and to determine its associations with potential clinical and disease activity factors. This was a cross-sectional study involving women with rheumatoid arthritis between the ages of 20 and 60 years. A validated Malay Version Female Sexual Function Index (MVFSFI) was administered to diagnose FSD. Sociodemographic and disease activity profiles were obtained and those who had and did not have FSD were compared. Among 63 respondents, 51 patients were included in the analysis for FSD. The prevalence of FSD in women with rheumatoid arthritis attending UKMMC and Hospital Putrajaya Rheumatology Clinic was 29.4%. Erythrocyte sedimentation rate (ESR) and Disease Activity Score in 28 joints (DAS28-ESR) correlates with MVFSFI score with r = −0.364 (P = 0.

Cardiovascular disease (CVD), a commonly used term for diseases o

Cardiovascular disease (CVD), a commonly used term for diseases of the heart and blood vessels, is the number one cause of death world-wide [1]. It is projected that annual global cardiovascular deaths will increase

from 16.7 million in 2002 to 23.9 million by 2030 [1]. The selleck chemical HIV pandemic has contributed significantly to mortality rates in many countries over the past three decades. However, the introduction of effective antiretroviral therapy (ART) has substantially reduced AIDS-related mortality [2, 3] and thus non-HIV-related mortality, such as that attributable to CVD, has become increasingly important for the estimated 33.3 million people living with HIV (PLHIV) [4, 5]. There is no consensus on the risk of CVD associated with HIV infection and the use of ART [6, 7]. Therefore, in this study we conducted a systematic review and meta-analysis of the published literature to assess the relative risk (RR) of CVD among PLHIV compared with the HIV-uninfected population. We also investigated the RR of CVD associated with the use and duration of ART, including different classes of ART drugs administered.

We conducted a comprehensive literature search of the peer-reviewed mTOR inhibitor publications through Medline, during July–November 2010, and conference proceedings of the Conference on Retroviruses and Opportunistic Infections (CROI) and International AIDS Society with the following search keywords: ‘HIV or human immunodeficiency Phosphatidylinositol diacylglycerol-lyase virus or AIDS or acquired immunodeficiency syndrome’ AND ‘cardiovascular or CVD or myocardial infarction or heart disease or vascular disease or coronary artery disease or coronary heart disease or myocarditis or cardiomyopathy or cardiac disease or cardiac arrhythmias’ AND ‘relative risk or risk ratio or RR or odds ratio or OR or hazard ratio or HR or incidence’. We included

cohort studies and randomized controlled trials that reported HIV-infected adults in at least one study arm. We categorized studies that reported on ART according to the three major drug classes [protease inhibitor (PI), nonnucleoside reverse transcriptase inhibitor (NNRTI) and nucleoside reverse transcriptase inhibitor (NRTI)] compared with the outcome among PLHIV not on ART. The primary outcome for our analysis was the incidence of CVD. For the purpose of this review, CVD includes myocardial infarction (MI), ischaemic heart disease (IHD), cardiovascular and cerebrovascular disease (CVD) and coronary heart disease (CHD). Studies that estimated the risks using incidence rate ratio (IRR), relative risk (RR), odds ratio (OR) or hazard ratios (HR) were included. We screened the titles of all articles for appropriateness, followed by the abstract, before retrieval of the full text. Studies that reported HIV and/or AIDS and CVD, and provided estimates of risk factors or estimates of RR, were included in the analysis.

3%, and in flooded pots, it was 163% (all significantly

3%, and in flooded pots, it was 16.3% (all significantly

different from the null hypothesis), indicating that there was a negative correlation between the competitiveness of the nonmotile mutant and vermiculite water content. Hence, we evaluated the competition for nodulation of all strains in the flooded condition. As shown in Table 2, the behavior of the mutants carrying one flagellum was similar as in field capacity (except LP 6866, which, although occupied 64.3% of nodules, did not deviate significantly from the null hypothesis due to higher experimental variability). As in field capacity, LP 3008 seemed to compete better than LP 3004 against its derivative without a thin flagellum. Meanwhile, the nonmotile double mutants

were again significantly less competitive than in field capacity. Bacterial swimming may be observed in semi-solid agar plates as a colony expansion a this website click here few millimeters below the agar surface, and must not be confused with swarming, which occurs in plates of more concentrated agar where colonies of differentiated cells move on the surface (Harshey, 1994, 2003). Indeed, rhizobia mutants able to produce swimming halos, but swarming colonies were not described (Braeken et al., 2007; Nogales et al., 2010). Our results showing swimming in 0.3% agar indicated that the thin flagellum of B. japonicum is actively used for this motion, because LP 5844 (ΔfliC1-4, producing only the thin

flagellum) formed the widest swimming halo of all mutants. In addition, this strain tumbled more frequently than the wild type. In agreement with our results, Wolfe & Berg (1989) also reported that the swimming halo rate of expansion increases with Urocanase tumble frequency. Thin flagellum derepression in LP 3008 may also cause its faster spread in 0.3% agar; however, it does not explain why the LP 3008 mutant lacking this flagellum still formed wider swimming halos than the corresponding mutant in the LP 3004 background. In 0.3% agar, the consumption of nutrients and release of other chemicals by the rings of bacteria moving inside the medium creates a chemoattractant gradient (Adler, 1966). Thus, the higher chemotaxis of LP 3008 (Althabegoiti et al., 2008) may also contribute to its higher displacement. After characterizing the motility provided by each flagellum, we assessed their roles in the competition for nodulation in vermiculite. Although all mutants moved less than the parental strains in swimming plate assays, they were differently affected in their competitiveness for nodulation, which also depended on the water status of the vermiculite. While mutants lacking the thin flagellum were, in general, more competitive than the parental strains both at field capacity and in the flooded environment, the mutants lacking the thick flagellum were less competitive.