aeruginosa was supplied to the growth medium (McClean et al., 1997). Vibrio harveyi bioassay strain BB170 was purchased from Guangdong Institute of Microbiology, China, and was grown in autoinducer bioassay medium to determine the presence of AI-2-like molecules in the dichloromethane extracts of M. aeruginosa by examination of the bioluminescence (Bassler et al., 1997). AHLs were studied by LC-MS on a C18 stationary phase column [150 × 2.1 mm, Patricle Sz. (u) Dim.]. The S1P Receptor inhibitor mobile phases

consisted of water (A) and acetonitrile (B) at a flow rate of 0.2 mL min−1. The organic content in the gradient was increased from 15% B to 65% B over 40 min and then to 15% B over 5 min with an additional 5 min at 15% B. Injection volume was 10 μL, and UV detection was set at 210 nm. The eluent from the HPLC was linked directly to a liquid chromatography (LCQ) Advantage MAX mass spectrometer (Finnigan). For identification of AHLs, the mass spectrometer was operated in full-scan mode from 50–800 Da to determine whether any signals indicative of the compounds could be detected. AHLs were regarded Napabucasin as being present only if the HPLC retention time, the full-scan

MS, and subsequent fragmentation analysis were in agreement with those of the reported AHLs (Sharif et al., 2008). Algal cells for SEM observation were collected from the abovementioned 1000-mL culture of M. aeruginosa at 10, 20, 30, and 40 days after inoculation and prepared according to the method described by Chen & Yeh (2005). Basically, the algae cells were filtered through a 0.45-micron nylon membrane filter. Then, the membrane filters were fixed with 2.5% gluteraldehyde at 4 °C overnight, washed with PBS buffer (pH7.0), and dehydrated with successive increasing different concentrations of ethanol. The dried samples were Pyruvate dehydrogenase mounted on copper stubs and sputter coated with

gold–palladium and observed using a scanning electron microscope (JEOL-JSM-6490, Japan). Detection with three bioreporters showed that both C. violaceum CV026 and V. harveyi BB170 exhibited a negative reaction, while A. tumefaciens KYC55 revealed a positive reaction when they were cultured with the addition of the dichloromethane extracts of M. aeruginosa at 10, 20, and 30 days after inoculation. Based on specific targets of the three biosensors, the results demonstrated that M. aeruginosa could produce QS signals that belonged to an autoinducer-1 (AI-1) with a long chain. The relative concentrations of QS signals in the metabolites of M. aeruginosa at given growth phases were measured based on the β-galactosidase activity of strain KYC55 when they were treated with AHL compound N-3-oxo-octanoyl homoserine lactones (OOHL). Results showed that the concentration of QS signals in the metabolites of M.

, 1989; Ward et al., 2008). Most of the biosynthesis pathways of trichothecenes are regulated by Tri5 genes found within the 25-kb Tri cluster (Kimura et al., 2003). Fusarium graminearum-specific Fg16NF/R (Nicholson et al., 1998) and trichothecene strain-specific Tox5-1/2

(Tri5 genes) primer sets were designed (Niessen & Vogel, 1998) to assess FHB outbreaks and the impact of mycotoxic strains on the environment (Wu et al., 2002). Aside from affecting the quality of crops and grains, FHB outbreaks are a source of toxigenic trichothecene contaminants that cause neurotoxicity, severe toxicoses, vomiting, food/feed refusal and immunosuppression in humans and animals (Vasavada & Hsieh, 1987; Edwards Selleck GDC0068 et al., 2001; Lutz et al., 2003; Leslie & Summerell, 2006). Thus, controlling the spread of FHB in crops, in particular FHB associated to F. graminearum outbreaks, is crucial to prevent the negative impact of mycotoxin accumulation in food and feed. Many scientists regard biological control as a promising environmental approach (Pal & McSpadden, 2006) and a practical option to combat Fusarium Wnt drug pathogenic strains (Vujanovic, 2008).

Most biocontrol agents studied as well as commercially available biopesticides use beneficial bacterial strains and necrotrophic mycoparasitic fungi, such as Trichoderma harzianum Rifai, against Fusarium (Khan et al., 2006). However, Ixazomib their efficiency in controlling Fusarium is limited and the outcomes are disputed. Relatively little information is available on the potential of biotrophic mycoparasitic fungi as biocontrol agents to manage F. graminearum

outbreaks. This could be due to the nature of biotrophic mycoparasites, which have a narrower host-specificity (Cortes-Penagos et al., 2007) as well as difficulties encountered when growing them on artificial or agar media. Although several biotrophic mycoparasites have been reported in association with Fusarium (Gliocephalis, Melanospora, Persiciospora, Stephanoma and Sphaerodes), none was noted to parasitize F. graminearum (Hoch, 1978; Davanlou et al., 1999; Harveson & Kimbrough, 2001a, b; Jacobs et al., 2005). Recently, Sphaerodes mycoparasitica Vujanovic biotrophic mycoparasite was isolated and identified from Canadian fields in association with Fusarium oxysporum, Fusarium avenaceum and F. graminearum (Vujanovic & Goh, 2009). Sphaerodes mycoparasitica was found to be a fusion and haustorial-like biotrophic mycoparasitic fungus of F. oxysporum and F. avenaceum (Goh & Vujanovic, 2010). In this study, S. mycoparasitica is reported, for the first time, as a biotrophic mycoparasite of 3-ADON- and 15-ADON-producing F. graminearum strains. This biotrophic mycoparasite is also an efficient suppressor of growth and reducer of the amount of DNA of mycotoxigenic F. graminearum strains in dual-culture mycoparasite–Fusarium assays.

2), with most isolates sampled from the same host grouping together. In support, the host is known to have a significant impact on the genetic structure of pathogen populations, especially in pathosystems characterized by the rapid breakdown of race-specific resistance (McDonald et al., 1989). Finally, while Newton et al. (2001) and Bouajila et al. (2007) indicated no clear relationship between genetic and pathogenic variation using RAPD and AFLP markers, the calculated degree of coincidence between pathotype and SSR haplotypes (Table 4) allowed the determination of pathogenicity in 52% of the isolates by fingerprinting with seven microsatellite loci. A similar

discrepancy in the SSR haplotype and pathogenicity has also been reported MAPK inhibitor by Takeuchi & Fukuyama (2009). In addition, many SSR alleles were shown to be linked to virulence (Table 3). These may serve as rapid

molecular tools for pathogen detection, without the inoculation that requires long incubation periods before ultimate disease assessment. This investigation was cosponsored by ICARDA-ETH Zurich. The authors acknowledge the support and the use of facilities of ETH – Institute of Integrative Biology ‘Phytopathology Group’, where this work was carried out. We are grateful to Dr Bruce for providing SSR primers. “
“The plant hormone ethylene has been reported to inhibit the Agrobacterium tumefaciens-mediated transformation efficiency of many plants. In this study, an acdS gene that encodes 1-aminocyclopropane-1-carboxylic acid (ACC) deaminase, an enzyme that selleck chemicals llc breaks down ACC, the direct precursor of ethylene biosynthesis in all higher plants, was introduced into A. tumefaciens GV3101∷pMP90. It was found that the presence of active ACC deaminase in A. tumefaciens reduced ethylene levels produced by plant tissues during the process of infection PRKD3 and cocultivation, and significantly increased the transformation efficiency of three commercial canola cultivars: Brassica napus cv. Westar, B. napus cv. Hyola 401 and B. napus cv. 4414RR. Agrobacterium tumefaciens is an important tool for plant genetic engineering. However, the low

transformation efficiency of many commercially important crops is the main factor limiting its use. Among various factors, ethylene produced by plants is one that inhibits A. tumefaciens-mediated transformation efficiency. For example, it has been reported that reducing the ethylene level increased the expression of the vir genes of A. tumefaciens, thereby increasing gene delivery efficiency (Nonaka et al., 2008a). Moreover, application of ethylene inhibitors such as aminoethoxyvinylglycine or silver ions in the tissue culture medium has been reported to improve the transformation efficiency of many plant species, such as bottle gourd, cauliflower, apricot and apple trees (Chakrabarty et al., 2002; Burgos & Alburquerque, 2003; Han et al., 2005; Petri et al., 2005; Seong et al., 2005).

Our study suggests that measures of concordance should be revised to incorporate items that measure

the doctor’s contribution in making the decision as well as in encouraging the patient to be involved in the decision. The adapted scale, with good inter-item reliability, could be used as a concordance measure in HIV clinics. The study had limitations. First, only patients’ perspectives and characteristics were measured and there was no information on the individual doctors [35] or from independent observers. Secondly, the study did not aim to determine causality. It is therefore possible that patients in better health perceived their communication with doctors as more concordant. One study found that patients with less intense symptoms were more satisfied with their care [36], although this finding was not replicated in a later study Quizartinib mouse [37]. However, research has shown C59 wnt manufacturer that patients with better self-rated health were more likely to be consumerist [38] and thus likely to have higher expectations of medical care, which should lead to perceiving doctors as less concordant. Research using intervention trials has shown that increased patient involvement in the medical

consultation results in better health outcomes in patients with ulcers and diabetes [39,40]. Our study demonstrated that overall concordance was related to CD4 cell count 6–12 months post-study after the baseline CD4 cell count was controlled for, suggesting a potential causal link between concordance and health outcomes. Further

research is needed to determine causality and to investigate possible mechanisms such as greater adherence, greater perceived control over illness and reduced anxiety/depression. Thirdly, our Sitaxentan limited sample size and restricted geographical study locations make it difficult to generalize from our findings. White homosexual men who were university educated and born in the United Kingdom were more likely to complete the Concordance Scale. However, no relationship was found between these demographic factors and concordance. Differences between completers and noncompleters were also found in terms of CD4 cell count and VL, but these disappeared once we controlled for stoppers being less likely to complete the scale. Moreover, symptom, adherence and quality of life variables did not differ between completers and noncompleters. It should also be noted that the five participating clinics account for a large proportion of UK patients, but may not necessarily be representative of all NHS providers of HIV care in the United Kingdom, nor reflect all clinician styles. This study supports the importance of patients’ reports of concordance in terms of health and health-related outcomes within HIV care. Further research is needed to establish causality by conducting intervention studies.

All but one were immigrants Ruxolitinib in vivo with AIDS as underlying condition (97%). One patient was an oncohematological patient (Table 2, patient 11) and was classified as a possible case. The other 29 cases were classified as proven (97%). The culture was positive in 73% of patients (22 cases) but always several weeks after the onset of symptoms. In seven cases (23%) the fungi was not cultured and the yeast cells were visualized in the tissues. The immunodiffusion test was performed in sera from 20 patients and was positive in only eight patients (40%). RT-PCR was performed in samples from

27 patients and was positive in 24 patients, showing a sensitivity of 89%. By samples, RT-PCR was performed on 54 samples from these patients: 16 sera, 10 respiratory samples, 8 blood samples,

6 biopsies, 6 bone marrow BMS-734016 samples, 4 plasma samples, 3 lymph node biopsies, and 1 cerebrospinal fluid. The RT-PCR was positive in 11 sera (69%), 10 respiratory samples (100%), 3 blood samples (37.5%), 6 biopsies (100%), 4 bone marrow samples (67%), three plasma samples (75%), and two lymph nodes (67%). Results were obtained within 24 hours of receiving the samples. When the fungus had been cultured, DNA was extracted from mycelia to perform PCR amplification and sequencing of ITS regions. All sequences matched with H capsulatum. We obtained the variety duboisii in three patients from African countries (Table 2; patients 7, 29, and 30). We had six patients with proven PCM. The fungus was cultured only in one patient several weeks after receiving the sample (CNM-CM5413). In the other cases characteristic budding yeasts were observed in clinical samples. The immunodiffusion test was performed in sera from five patients

and was positive in all cases (100%), although the signal was very weak in three of them (60%). RT-PCR was performed on samples from these six patients and was positive in all cases (100%). By samples, RT-PCR was performed on four tissue biopsies, four serum samples, three blood samples, two sputum samples, one bronchoalveolar lavage (BAL), and one lung biopsy. RT-PCR was positive in two blood samples (66%), two sputum samples (100%), four biopsies (100%), one BAL (100%), and one lung biopsy Methisazone (100%). The RT-PCR results were also obtained 24 hours after receiving the samples. DNA was extracted from the isolated strain (CNM-CM5413) to perform a PCR amplification of the ITS region, followed by sequencing. The sequence matched with P brasiliensis. In two patients, we tested samples several weeks after starting the antifungal therapy, showing that the amount of DNA had either decreased or disappeared.25 Diagnosis of histoplasmosis and PCM is very frequently hampered by a lack of experience in non-endemic areas.

Then, the phage suspension and its several dilutions were spotted on the soft

agar lawns and incubated at 37 °C for 18–24 h. Fifty phage-resistant clones were picked from the lysis zone formed by the phage on A. baumannii lawns from seven different plates. The clones were subjected to three cycles of purification, resuspended in a saline solution, treated with chloroform, and centrifuged. Supernatants were spotted on the phage-sensitive A. baumannii lawn. Also each resistant clone was grown in 30 mL LB broth in the presence of mitomycin C (0.3–1 μg mL−1). The samples were cleared by low-speed centrifugation (7000 g for 30 min.), and supernatants were concentrated 100–1000 times by ultracentrifugation at 4 °C for 2 h (85 000 g; Beckman SW28 rotor). The presence or absence of the phage was estimated by electron microscopy. LY2835219 in vivo A putative prophage in the genomic DNA of the resistant clones was looked for using multiplex PCR

with two pairs of primers specific to phage AP22 DNA, developed on the base of partial sequence of the phage genome. These were AP22A-f (5′-AGTTCGTTCTGCTGTTTGG-3′) and AP22A-r (5′-TCCTCAACATACCAAATCG-3′); AP22B-f (5′-GTGTTCATTTCGTTCTCTCA-3′) and AP22B-r (5′-CGACATTTCTCAACATCAGC-3′). As control of the PCR, primers for the gene 16S rRNA gene of A. baumannii were used. Exponentially grown A. baumannii cells were mixed with the phage (MOI = 0.001) and incubated at room temperature. A volume of 100 μL of samples Buparlisib in vitro was taken in 1, 2, 3, 4, 5, 10, 15, and 20 min Pembrolizumab cost and mixed then with 850 μL of SM buffer supplemented with 50 μL of chloroform. After centrifugation, the supernatants were titrated for further determination of unadsorbed phages by the double-layer method at different time intervals. The adsorption constant was calculated according to the study by Adams (1959) for a period of 5 min. A volume of 20 mL of host bacterial cells (OD600 nm of 0.3) was harvested by centrifugation (7000 g, 5 min, 4 °C) and resuspended in 0.5 mL LB broth. Bacterial cells were infected with the phage at MOI of 0.01. The bacteriophage was allowed to adsorb for 5 min at 37 °C.

Then, the mixture was centrifuged at 13 000 g for 1 min to remove unadsorbed phage particles, and the pellet was resuspended in 10 mL of LB broth. Samples were taken at 5-min intervals during incubation at 37 °C within 2 h and immediately titrated. The procedure was repeated three times. Latent period was defined as the interval between adsorption of the phage to the host cell and release of phage progeny. The burst size of the phage (the number of progeny phage particles produced by a single host cell) was expressed as the ratio of the final count of released phage particles to the number of infected bacterial cells during latent period. The bacteriophage (108 PFU mL−1) was incubated in 1 mL of pH buffers at pH 2, 4, 7, 9, and 12 at room temperature. Samples were taken in 1, 3, 6, and 24 h and titrated using the double-overlay method.

The results are presented as the difference in the average cycle threshold (ΔCt) with the control rpoD gene. Statistical

comparisons were performed by an anova and Tukey’s post-tests using prism 4.0 software (Graphpad Software). Total RNA (2.5 μg) Ruxolitinib cell line isolated from a culture of 2787 at an OD600 nm of 2.0 was converted to cDNA using the High-Capacity cDNA Reverse Transcription Kits (Applied Biosystems) according to the instructions of the manufacturer. PCR reactions were performed on the cDNA using the primers promo-R (5′-ACAATATGTTTCCTGACTCCTCAT-3′) and promo1-F (5′- ATTAGATTAACAAAAAGGATAACGTCAGATCT-3′), promo2-F (5′-CTTTTATTCGCCACGACACAAG-3′), promo3-F (5′-CCGTTCTAGTTATCTTGGATATTACATTAT-3′) or promo4-F (5′-TATTACATTATATAGGAGGGATTATGACTTTC-3′). The PCR amplification products were visualized on an agarose gel. RACE was performed using the 5′ RACE System, version 2.0 (Invitrogen), according to the instructions of the manufacturer with 3 μg of RNA extracted from E. coli 2787 grown to an OD600 nm this website of 0.7 or 2.0, with

gene-specific primers RACE_aah1 (5′-GGCTGGTTATCCGTATCGCC-3′), and RACE_aah2 (5′-CCAATTCTGTACGTTGCATAAGGC-3′) or RACE_aidA1 (5′-TGATATTTGTACTATCAGTTATACCTCCTG-3′ and RACE_aidA2 (5′AATCGTCTGATTTCCACCGC-3′). The amplified products were analyzed by agarose gel electrophoresis and sequenced. Samples of bacterial cultures were drawn at several times during growth and normalized at the same OD600 nm. The bacteria were pelleted and resuspended in 50 mM Tris-HCl, pH 7.5,

150 mM NaCl (TBS). Whole-cell samples were then diluted in twice-concentrated SDS-PAGE loading buffer Florfenicol containing β-mercaptoethanol, and denatured by heating at 100 °C for 10 min. The samples were then separated by SDS-PAGE on 10% acrylamide gels and transferred to polyvinylidene fluoride membranes (Millipore). Immunodetection was performed with a serum raised against glycosylated heat-extracted mature AIDA-I (Charbonneau et al., 2006) or antibodies against GroEL protein (Sigma). Immune complexes were revealed using secondary antibodies coupled to horseradish peroxidase and 3,3′,5,5′-tetramethylbenzidine (Sigma). Using primers extending upstream of aah and downstream of aidA, we completely sequenced the insert of plasmid pIB264 (Benz & Schmidt, 1989). The insert is 6241 nucleotides long, with a G+C content of 44.6% and the sequence has been deposited in GenBank (GU810159). The sequence upstream of aah reveals the 5′-end of an ORF (Fig. 1).

parapsilosis (Kurnatowski et al., 2007; Medeiros et al., 2008; Pires-Goncalves et al., 2008). Addition of saliva

significantly promoted Candida growth (P < 0.0001) as compared with control values (Fig. 1). A 1–2.3 log(10) increase in CFU was observed in C. parapsilosis incubated with 1–20% (v/v) saliva (P < 0.0001). No difference in the survival of C. parapsilosis with either 1% or 5% (v/v) saliva was seen, whereas 20% saliva induced a significant increase in CFU counts [> 2 vs. 1 log(10) CFU mL−1 increase; P < 0.0001]. Survival of C. albicans without saliva steadily decreased with time; a 3 log(10) CFU mL−1 decrease was observed after 15 days MG-132 clinical trial (P < 0.0001) (Fig. 1b). As expected, tap water was not an appropriate medium for C. albicans, which required

a more protected environment to optimize its growth. Our results suggested that addition of saliva to the medium could provide some essential components to C. albicans: when compared with control, at each time point, a low increase [<1 log(10) CFU mL−1; P < 0.0001] was indeed observed during the 360 h of incubation in the presence of 1% (v/v) saliva. In fact, our results suggested that 1% (v/v) saliva promoted C. albicans yeast survival but was not able to induce their proliferation. On the other hand, 5% and 20% (v/v) saliva induced a strong growth increase of about 1–2.5 and 2–3.5 log(10) CFU mL−1, respectively (P < 0.0001); the log(10) increase in CFU observed with 5% and, in particular, 20% [2–3.5 log(10) CFU mL−1] was obvious from the first day of the test and was then stable and persistent throughout the 15-day period. Finally, check details C. glabrata was the most susceptible species in tap water and was unable to survive for more than 192 h if saliva concentration was <20% (v/v) (Fig. 1c). The addition of 20% (v/v) saliva to tap water induced an increase of 2.3–4.5 log(10) CFU mL−1 (P < 0.0001), whereas the effect of 1% and 5% saliva, although clearly positive

during the first 72 h, then became less clear. The effect of saliva on C. albicans has been investigated in the mouth environment by Celecoxib several authors who suggested potential interactions but also highlighted conflicting observations. For example, it has been shown that whole saliva promoted adherence to silicon in a dose-dependent manner (Holmes et al., 2006). Other authors showed decreased biofilm formation in the presence of saliva (Jin et al., 2004). More recently, Elguezabal et al. (2008) showed a dual role played by whole saliva in decreasing the adhesion of germ-tubes but increasing that of yeast cells to polymethylmetacrylate. On the other hand, Leito et al. (2009) demonstrated that saliva could induce transition of hyphae to yeast forms in the mouth and may thus contribute to the oral defence against candidiasis; however, inhibition of the germination of C. albicans by whole saliva was not confirmed by Elguezabal et al.

Visual mismatch negativity was identified if, within the 100–300-ms latency range, deviant-minus-standard amplitude difference was different from zero at least at five subsequent points at any occipital location [for reviews of the characteristics of the range and surface distribution of the vMMN, see Czigler (2007) and Kimura (2011)]. In this

way, we identified an earlier (112–120 ms) and a later (284–292 ms) range of the difference potentials. At six electrode locations (PO3, POz, PO4, O1, Oz, and O2) as regions of interest, the average amplitude values of these epochs were calculated, and entered into anovas with factors of probability (deviant or standard), anteriority (parieto-occipital or occipital), and laterality (left, midline, or right). We compared, at the same electrode locations, the peak latencies and scalp distributions of the exogenous components and the difference potentials. Note that, Quizartinib at lower half-field stimulation, the C1 and C3 components are positive and the C2 component is negative. Investigation of the relationship between a negative component and the vMMN is relevant,

because it is important to separate the refractoriness/habituation of an exogenous activity from vMMN. In this context, the similar analysis of the positive components (C1 and C3) is less important, FG-4592 chemical structure because reduced exogenous positivities elicited by the deviant stimuli cannot be expected (in the case of stimulus-specific refractoriness/habituation, second amplitude reduction is expected, i.e. positive deviant-minus-standard difference). Peak latencies were measured at the maxima of the components. The distributions of the difference potential and the C2 component were compared with vector-scaled amplitude values (McCarthy & Wood, 1985). Where appropriate, Greenhouse–Geisser correction was applied. Effect size was characterised as partial eta-squared (η2). Post

hoc analyses were performed with Tukey’s HSD test. In the reported effects, the alpha level was at least 0.05. Participants avoided the red ship with a frequency of 82% (standard error of the mean, 1.53%), and caught the green ship with a frequency of 83% (standard error of the mean, 1.05%). This difference was not significant. There was no also difference in performance between the random and symmetric standard conditions. Figure 2 shows the ERPs elicited by the symmetric (A) and random (B) stimuli, as both standards and deviants, and also the deviant-minus-standard difference potentials. The stimuli elicited a positive–negative–positive (C1–C2–C3) set of pattern-specific exogenous components (Jeffreys & Axford, 1972). Table 1 shows the latency values of the exogenous components, and Fig. 3 shows the scalp distribution of the C1, C2 and C3 components and the difference surface distributions.

It is also used as part of combination formulations for rice (Singh et al., 2008; Saha & Rao, 2009). Chlorimuron-ethyl

CYC202 solubility dmso exerts carry-over effects on succeeding crops such as sugar beet, corn and cotton. It reduced the yield of sugar beet planted 1 year after its application (Renner & Powell, 1991). Chlorimuron-residue haremed corn (Curran et al., 1991), and also harmed sunflower, watermelon, cucumber and mustard when observed 16 weeks after application (Johnson & Talbert, 1993). Although its persistence is moderate in soil [half-life (T1/2) 30 days], like many other sulfonylurea herbicides, its persistence increases with increasing pH. The T1/2 of chlorimuron under acidic conditions (pH 5) is 17–25 days, whereas at higher pH this may increase to 70 days. The half-life of chlorimuron in a silt-loam soil was 7 days at pH 6.3 and 18 days at pH 7.8 (Brown, 1990). By using a root bioassay technique, Schroeder (1994) determined the half-life of chlorimuron in soils of different pH-ranges as 12–50 days. Bedmar et al. (2006) observed a wide range of half-life for chlorimuron in soil from 30 days at pH 5.9 to 69 days at pH 6.8. Chlorimuron-ethyl degrades in the agricultural environment primarily via pH- and temperature-dependent chemical hydrolysis (Beyer et al., 1988; Brown, 1990; Hay, 1990), as observed for many sulfonylurea herbicides, such as sulfometuron-methyl (Harvey et al., Ganetespib in vivo 1985),

chlorsulfuron (Sabadie, 1990), metsulfuron-methyl (Sabadie, 1991), rimsulfuron (Schneiders et al., 1993), nicosulfuron (Sabadie, 2002) and flazasulfuron (Bertrand et al., 2003). The phototransformation of chlorimuron by sunlight also takes place on the soil (-)-p-Bromotetramisole Oxalate surface (Choudhury & Dureja, 1996a) and in water (Venkatesh et al., 1993; Choudhury & Dureja, 1996b). Within the surface soil chlorimuron is also considered to serve as a source of carbon, nitrogen and sulfur for microorganisms. There are reports on the utilization of sulfonylurea herbicides by microorganisms. The metabolic pathways for the degradation of chlorsulfuron and metsulfuron-methyl

by Streptomyces griseolus (Joshi et al., 1985; Reiser & Steiglitz, 1990), and trisulfuron by S. griseolus in artificial media (Dietrich et al., 1995) have been established. At low pH the degradation of trisulfuron-methyl takes place by chemical hydrolysis, whereas in neutral to alkaline soil, microorganisms play the dominant role in its degradation (Peeples et al., 1991), and the major degradation route is cleavage of the sulfonylurea bridge (Vega et al., 2000). Streptomyces griseolus can also de-esterify and O-dealkylate the chlorimuron-ethyl molecule (Reiser & Steiglitz, 1990). A bacterium, Pseudomonas sp., isolated from chlorimuron-ethyl-contaminated soil degrades the herbicide by cleaving the sulfonylurea bridge (Ma et al., 2009), and a yeast strain, Sporobolomyces sp., was isolated as a chlorimuron-degrading organism (Xiaoli et al., 2009).