, 2009). For Cry3A protein (the most important coleopteran-specific Cry toxin), loop 1 has an important function in biological activity: the mutations AZD4547 R345A, Y350F, Y351F, ΔY350 and ΔY351 showed higher levels of toxicity against Tenebrio molitor (Coleoptera) (Pardo-López et al., 2009). SN1917 has several changes related to these observations, with respect to the parental Cry1Ba (R345Q, Y349M and ΔY350). It may be that these residues are important factors of activity, for example arginine has a positive

charge because the guanido group is ionized over the entire pH range in which proteins exist naturally, and the hydroxyl group of the phenolic ring of tyrosine residues makes this aromatic ring relatively reactive in electrophilic substitution reactions (Creighton, 1993). On the other hand, anticoleopteran Cry proteins are only toxic after in vitro solubilization, probably because the protoxin cannot be solubilized at the neutral to weakly acidic gut pH of Coleoptera (de Maagd et al., 2001). For the midgut and the hindgut of CBB, values between pH 4.5

and 5.2 were consistently observed (Valencia et al., 2000). This result suggests that there is an important activity determinant in selleck inhibitor domain II of Cry1Ba, although it may be a nonspecific binding. For this reason, further study of CBB physiological conditions and mutagenesis Megestrol Acetate site-directed in this toxin and other related Cry proteins is necessary.

The authors are grateful to Dr Ruud A. de Maagd for his participation to this project and the critical discussion of this paper. This work was supported by Dirección de Investigación de la Universidad Nacional de Colombia sede Bogotá (Colombia). S.A.L.-P. gratefully acknowledges Colciencias for his PhD fellowship. “
“The SbmA protein is involved in the transport of MccB17-, MccJ25-, bleomycin- and proline-rich peptides into the Escherichia coli cytoplasm. sbmA gene homologues were found in a variety of bacteria. However, the physiological role of this protein still remains unknown. Previously, we found that a combination of sbmA and tolC mutations in Tn10-carrying E. coli K-12 strains results in hypersusceptibility to tetracycline. In this work, we studied sbmA expression in a tolC mutant background and observed an increased expression throughout growth. We ruled out the global transcriptional regulator RpoS and the small RNA micF as intermediates in this regulation. The tolC mutation induced the expression of other well-characterized strong σE-dependent promoters in E. coli.

, 1990). Trametinib The psaA gene is transcribed in the psaEFABC operon of Y. pestis and Y. pseudotuberculosis, with psaEF encoding the activator/sensor proteins, whereas psaBC encodes the chaperone/usher proteins (Lindler & Tall, 1993; Yang & Isberg, 1997). This operon is homologous to the myfEFABC locus of Y. enterocolitica (Iriarte et al., 1993). The signal

peptide of Y. enterocolitica MyfA was identified (Iriarte et al., 1993) and needs to be determined for PsaA in both Y. pseudotuberculosis and Y. pestis. In bacteria, a signal peptide present on proteins that are destined to be secreted or to be membrane components, it is usually present at the amino terminal and absent from the mature protein. The signal peptide is removed by signal peptidases (SPases)

as an SPase-I or SPase-II (processing of prolipoproteins) (Yamaguchi et al., 1988; Tuteja, 2005). Recently, a new generation of improved recombinant attenuated Salmonella Typhimurium vaccine (RASV) strains, such as Salmonella enterica serovar Typhimurium χ9558, have been developed and tested using heterologous antigens (Li et al., 2009). These RASV strains will facilitate investigations into the role of selected amino acids in the biogenesis of Y. pestis PsaA. The focus of this present Crizotinib study is a better understanding of the PsaA translocation process and improvement of its secretion, with the eventual goal of developing a subunit vaccine against Y. pestis. Escherichia coli, Salmonella, Y. pestis strains and plasmids used in this study are listed in Table 1. Escherichia coli and Salmonella strains were grown in Luria–Bertani Avelestat (AZD9668) (LB) medium (1% Bacto tryptone, 1% NaCl, 0.5% yeast extract), 1.5% LB agar or on McConkey (Difco); when required, the medium was supplemented

with 50 μg mL−1 ampicillin, 10 μg mL−1 nalidixic acid, 0.2% mannose or 50 μg mL−1 diaminopimelic acid for growing the strain with ΔasdA mutation. DNA manipulations were carried out as described by Sambrook & Russell (2001). All primers (Integrated DNA Technology) were flanked with restriction enzymes (uppercase in the primer sequences), as shown in Supporting Information, Table S1. The psaEFABC genes were amplified by PCR from Y. pestis KIM6+ strain chromosome, and constructions were verified by DNA sequencing (Arizona State University Facilities). Fifteen codons from Y. pestis psaA were substituted with the most frequently used codons found in Salmonella genes for optimization of Y. pestis psaA expression in RASV strains. All amino acid substitutions and deletions in Y. pestis psaA were performed using a Quick-Change site-directed mutagenesis kit (Stratagene). The presence of a desired mutation was verified by DNA sequencing (Fig. 1a, Table 1). The recombinant PsaA-AU1-6XHis protein was overexpressed in E. coli strain LMG194, transformed with the pYA3883 (Table 1) and grown in 1 × minimal salts media (Curtiss, 1965), supplemented with 0.

Next, we examined the relationship between CAC and carotid lesion presence and FT among HIV-infected

participants using similar logistic regression models. In addition to the covariates mentioned above for the models including all participants, we adjusted for HIV clinical status and treatment parameters, including CD4 count >200 cells/μL, viral load >400 HIV-1 RNA copies/mL, and antiretroviral therapy status. Finally, we examined the relationship between IMT and FT among HIV-infected participants using a linear regression model adjusted for all factors mentioned above. Analyses were conducted using sas version 9.2 (SAS Institute, Cary, NC), and a two-sided P-value LY294002 supplier of < 0.05 was considered statistically significant. Table 1 presents the distribution of relevant demographic and clinical characteristics according to HIV status. The HIV-infected men (n = 534) were younger and had lower BMI than the HIV-uninfected men. The HIV-infected men were more likely to belong MG-132 mw to a race other than White and more likely to have hepatitis C virus (HCV) infection than the HIV-uninfected men. The mean LDL and HDL cholesterol values were higher in the HIV-uninfected group. Log HOMA-IR was higher in the HIV-infected men (P < 0.0001). In our sample, adjusted mean log FT was lower in HIV-infected men than in HIV-uninfected

men, with values being 4.49 and 4.62, respectively (P = 0.0004), corresponding to FTs of 88.7 and 101.7 ng/dL, respectively. FT was higher in HIV-uninfected individuals and decreased with age. The FT in an HIV-infected man was equivalent to the FT in an HIV-uninfected man 13 years older [β for HIV-infected vs. uninfected status: −0.13 (P < 0.001); β for age: −0.01 (P < 0.0001)]. The overall prevalence of CAC in HIV-infected and HIV-uninfected participants

was 32.5%. The adjusted odds ratio (OR) of CAC presence was 1.44 [95% confidence interval (CI) 0.92, 2.24] and the adjusted OR for carotid lesion presence was 1.69 (95% CI 1.06, 2.71) in HIV-infected men compared with HIV-uninfected men. There was no difference in the adjusted mean log carotid IMT between HIV-infected and HIV-uninfected men (Table 2). Table 2 shows the adjusted associations between log FT and CAC presence, carotid IMT, and carotid lesion presence in all study Dynein participants. In this analysis, FT was not associated with CAC presence, IMT, or carotid lesion presence. HIV-infected status was not associated with CAC presence or carotid IMT but was associated with carotid lesion presence (OR 1.69; 95% CI 1.06, 2.71). The ORs of CAC presence and carotid lesion presence for HIV-infected compared with HIV-uninfected men were similar, although only the OR of carotid lesion presence achieved statistical significance. Increasing age was positively associated with all three outcomes, and smoking was positively associated with CAC presence and carotid lesion presence. Elevated LDL cholesterol was positively associated with CAC presence in adjusted analysis.

Next, we examined the relationship between CAC and carotid lesion presence and FT among HIV-infected

participants using similar logistic regression models. In addition to the covariates mentioned above for the models including all participants, we adjusted for HIV clinical status and treatment parameters, including CD4 count >200 cells/μL, viral load >400 HIV-1 RNA copies/mL, and antiretroviral therapy status. Finally, we examined the relationship between IMT and FT among HIV-infected participants using a linear regression model adjusted for all factors mentioned above. Analyses were conducted using sas version 9.2 (SAS Institute, Cary, NC), and a two-sided P-value http://www.selleckchem.com/products/epacadostat-incb024360.html of < 0.05 was considered statistically significant. Table 1 presents the distribution of relevant demographic and clinical characteristics according to HIV status. The HIV-infected men (n = 534) were younger and had lower BMI than the HIV-uninfected men. The HIV-infected men were more likely to belong Thiazovivin purchase to a race other than White and more likely to have hepatitis C virus (HCV) infection than the HIV-uninfected men. The mean LDL and HDL cholesterol values were higher in the HIV-uninfected group. Log HOMA-IR was higher in the HIV-infected men (P < 0.0001). In our sample, adjusted mean log FT was lower in HIV-infected men than in HIV-uninfected

men, with values being 4.49 and 4.62, respectively (P = 0.0004), corresponding to FTs of 88.7 and 101.7 ng/dL, respectively. FT was higher in HIV-uninfected individuals and decreased with age. The FT in an HIV-infected man was equivalent to the FT in an HIV-uninfected man 13 years older [β for HIV-infected vs. uninfected status: −0.13 (P < 0.001); β for age: −0.01 (P < 0.0001)]. The overall prevalence of CAC in HIV-infected and HIV-uninfected participants

was 32.5%. The adjusted odds ratio (OR) of CAC presence was 1.44 [95% confidence interval (CI) 0.92, 2.24] and the adjusted OR for carotid lesion presence was 1.69 (95% CI 1.06, 2.71) in HIV-infected men compared with HIV-uninfected men. There was no difference in the adjusted mean log carotid IMT between HIV-infected and HIV-uninfected men (Table 2). Table 2 shows the adjusted associations between log FT and CAC presence, carotid IMT, and carotid lesion presence in all study Elongation factor 2 kinase participants. In this analysis, FT was not associated with CAC presence, IMT, or carotid lesion presence. HIV-infected status was not associated with CAC presence or carotid IMT but was associated with carotid lesion presence (OR 1.69; 95% CI 1.06, 2.71). The ORs of CAC presence and carotid lesion presence for HIV-infected compared with HIV-uninfected men were similar, although only the OR of carotid lesion presence achieved statistical significance. Increasing age was positively associated with all three outcomes, and smoking was positively associated with CAC presence and carotid lesion presence. Elevated LDL cholesterol was positively associated with CAC presence in adjusted analysis.

Omptins impact bacterial virulence by degrading or processing a number of host proteins or peptides (Haiko et al., 2009). Escherichia coli K12 OmpT was reported to efficiently degrade the AMP protamine (Stumpe et al., 1998). Other studies have shown that S. Typhimurium PgtE and Yersinia pestis Pla cleave α-helical AMPs such as C18G and human LL-37 (Guina et al., 2000; Galvan et al., 2008). CroP, the omptin of the murine enteric pathogen C. rodentium,

learn more was shown to degrade α-helical AMPs, including mCRAMP (Le Sage et al., 2009) (Fig. 1a). CroP-mediated degradation of AMPs occurred before they reached the periplasmic space and triggered a PhoPQ-mediated adaptive response. OmpT of enterohemorrhagic E. coli (EHEC) was shown to inactivate human LL-37 by cleaving it twice at dibasic sites (Thomassin et al., 2012). Galunisertib molecular weight Structures external to the bacterial cell envelope such as capsule polysaccharides (CPS), curli fimbriae,

exopolysaccharides involved in biofilm formation, and the O-polysaccharide of lipopolysaccharide play a role in AMP resistance. They are proposed to act as a decoy by binding AMPs and reducing the amount of AMPs reaching the bacterial membrane (Fig. 1b). Campos et al. (2004) reported that a K. pneumoniae CPS mutant is more sensitive to AMPs than the wild-type strain with a concomitant increase in AMP-mediated OM disruption, indicating that CPS acts as a shield against AMPs. Consistent with the cationic nature of AMPs, another study reported that only anionic CPSs decreased the bactericidal activity of AMPs (Llobet et al., 2008). A similar protective role for CPS was observed in Neisseria meningitidis. An unencapsulated serogroup B strain of N. meningitidis was more susceptible to the bacterially derived AMP polymyxin B, α- and β-defensins as well as the cathelicidins LL-37 and mCRAMP (Spinosa et al., 2007). Interestingly, sublethal concentrations of AMPs upregulated the transcription of the capsule genes in N. meningitidis, suggesting that increased capsule synthesis is a bacterial adaptation downstream of AMP sensing (Spinosa et al., 2007; Jones et al.,

2009). Bacterial exopolysaccharides are the major constituent of the extracellular biofilm matrix (Sutherland, 2001). Exopolysaccharides are most often Phosphatidylethanolamine N-methyltransferase anionic polymers that are proposed to play a role in the resistance of bacterial biofilms to innate host defenses. For example, the β-d-manuronate and α-l-guluronate polymer alginate produced by P. aeruginosa was shown to promote the formation of interacting complexes with LL-37 (Herasimenka et al., 2005). Pseudomonas aeruginosa alginate and exopolysaccharides from other lung pathogens were reported to inhibit the bactericidal activity of LL-37, indicating that sequestration of LL-37 by exopolysaccharides lowers the concentration of AMP at its target site (Foschiatti et al., 2009).

, 2000) and is expected to limit the extent of 14C-phenanthrene biodegradation in the soils; low TOC in soils can be an indication

of low microbiological activity (Margesin & Schinner, 2001). Samples taken in the selected sites were mostly bare of vegetation and plate counts revealed very low CFUs (Fig. 3) for both total heterotrophs and 14C phenanthrene-degrading bacteria. The presence of only small selleck compound numbers of PAH-degrading bacteria can be explained by the absence of degradation inducing chemicals from both biogenic and anthropogenic sources. Sufficient concentrations of biogenic volatile organic chemicals (VOCs) from plants (Wilcke, 2007; McLoughlin et al., 2009) and anthropogenic compounds have been identified as carbon sources for microbial activity, growth and the induction of appropriate genes for PAH degradation in indigenous microorganisms (Macleod & Semple, 2002; Johnsen & Karlson, 2005). Hydrocarbon degraders have been cultivated at levels > 105 cell g−1 from contaminated polar soils and have increased following oil spillage by 1–2 orders of magnitude in hydrocarbon contaminated soil compared with pristine soils (Aislabie et al., 2000). In this study, CFUs of 14C-phenanthrene-degrading bacteria increased in all five soils and by one order of magnitude in soils 1, 3 and 5 after mineralization in slurry selleckchem conditions (Fig. 3). Of the three temperatures

used in this study, 4 °C was the most representative of prevailing temperatures at Livingstone Island hence appropriate for optimum microbial activity. However, no significant amount of 14C-phenanthrene was mineralized in any of the five soils (Table 2). Reduced bioavailability of PAHs at low temperatures has also been reported as a possible reason for

low levels of microbial degradation (Eriksson et al., 2003). At low temperatures, the solubility and bioavailability of less soluble hydrophobic organic compounds, such as PAHs, decrease because of an increase in viscosity in the physical nature of the compounds and because of stronger sorption to the soil organic matter. Increased viscosity will decrease the degree of organic compound distribution (less surface area for microbial action) and subsequent diffusion rates to sites of biological action Venetoclax purchase leading to reduced extents of degradation (Nam & Kim, 2002). Ferguson et al. (2003a, b)obtained similar results when they found that mineralization of 14C-labelled octadecane was virtually absent at temperatures below or near the freezing point of water. At 12 °C, the extents of 14C-phenanthrene mineralized increased significantly in two of the five soils after a long lag phase. 14C-Phenanthrene was mineralized to a greater extent at 22 °C than at 4 and 12 °C for all the soils. The increasing solubility of phenanthrene with increasing temperature would mean that the amount of phenanthrene in solution (and therefore available for degradation) would have been higher at 22 °C that at 4 and 12 °C.

However, this association was not sustained by the observations obtained from the other two strains, where BALB/c had the greatest olfactory sensitivity but did not have the highest number of neuroblasts. Interestingly, a prior assessment of olfactory discrimination learning in 13 adult (10–18 weeks old) inbred mouse strains by

Brown and colleagues revealed that the C57BL/6J strain was capable of acquiring odor discrimination faster than most of the other strains including A/J (data available at the Mouse Phenome Database; MPD: 22531, 22532, 22570). Taking these data together, proliferation in RMS does not appear to be a good predictor of net OB neurogenesis, OB structure and function. Here, we considered the RMS as a discrete neurogenic structure and our results demonstrated GSK458 research buy the variable and heritable nature of cell proliferation in the RMS. A major QTL called Rmspq1 is identified on distal chromosome 11 for regulating the numbers of rapidly dividing precursors in the RMS but not in the SGZ. Furthermore, a subset of polymorphic genes underlying the Rmspq1 confidence interval have emerged as strong candidates due to their role in either cell cycle progression see more or involvement in signaling pathways known to regulate neural proliferation. Future analysis of these genes will include measuring the transcript

and protein abundance in RMS cells and correlating their expression profiles Protein kinase N1 with phenotypic data on the numbers of proliferating cells in the RMS, as well as determining the in vitro and in vivo functions of these genes in RMS proliferation. Overall, our study provides

strong evidence for the allelic effects on neural proliferation and a solid framework for further exploration of other genetic loci and gene variants that are part of the complex regulation of adult neurogenesis. Genetic insights gained from these studies may contribute to the future development of neural stem cell therapies used to compensate for the loss of neurons in neurodegenerative diseases and brain injuries (Elder et al., 2006; Maysami et al., 2008). This work was supported by NIH grants R01DA020677 to DG, AG18245 to DG, U01AA014425 to LL, P20 DA021131 to RW, and a grant from the Methodist Chair in Neuroscience to DG. We thank Derek Rains, Gurjit Rai, Meifen Lu, Richard Cushing, Erich Brauer and Alan Weatherford for their invaluable technical assistance. Abbreviations BrdU bromodeoxyuridine CV cresyl violet DG dentate gyrus GF growth fraction LOD likelihood of the odds LRS likelihood ratio statistic NSCs neural stem cells OB olfactory bulb QTL quantitative trait locus RI recombinant inbred RMS rostral migratory stream SGZ subgranular zone SVZ subventricular zone Tc total cell cycle time Ts S-phase time Fig. S1. Comparison of two BrdU-labeled cell counting methods for quantifying proliferative cells in the RMS.

This new concept derived from genome-wide phylogenetic analysis fits well with the physiological differences among the three genera, Gluconobacter, Gluconacetobacter, and Acetobacter, the latter two of which are found in similar habitats. Indeed, these genera

were previously classified as a single genus: Acetobacter. Yamada et al. (1997) separated the genus into Gluconacetobacter and Acetobacter on the basis of partial sequences of 16S rRNA gene. In contrast to the 16S rRNA gene-based phylogenetic tree, our results fit well with the fact that Gluconacetobacter and Acetobacter have similar physiologies and habitats. The present result clearly shows that concatenating large multiprotein Antiinfection Compound Library order dataset analysis is a very useful technique to improve the accuracy of phylogenetic inference. Although whole-genome sequences are needed, the technique should be useful for the analysis of phylogenetic relationships at the genome level. This work was supported by the Program for Promoting Basic Research Activities for Innovative Biosciences (PROBRAIN). Table S1. List of phylogenetic patterns of metabolic genes in Gluconobacter oxydans. Table S2. List of unique orthologous genes among Acetobacteraceae.

Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“The electron donor for periplasmic chlorate reductase of Ideonella dechloratans has been suggested to be a soluble cytochrome c.

BIBW2992 concentration We describe here the purification of the 9-kDa periplasmic cytochrome c, denoted cytochrome c-Id1, and demonstrate its ability to serve as an electron donor for purified chlorate reductase. The reaction rate was found to be linearly dependent on the cytochrome c concentration Leukocyte receptor tyrosine kinase in the range of 0.6–4 μM. A route for electron transport involving a soluble cytochrome c is similar to that found for other periplasmic oxidoreductases of the dimethyl sulfoxide reductase family, but different from that suggested for the (per)chlorate reductase of Dechloromonas species. Oxyanions of chlorine, such as chlorate (ClO3−) and perchlorate (ClO4−), have been introduced into the environment by human activities, for example through pulp and paper industrial effluents (Germgård et al., 1981). Both chlorate and perchlorate affect the marine environment by their toxicity to algae (van Wijk & Hutchinson, 1995). Since the beginning of the 20th century, it has been known that a wide variety of bacterial species (Logan, 1998; Richardson, 2000; Coates & Achenbach, 2004) decompose chlorate and perchlorate under anaerobic conditions. This activity is utilized in waste water treatment to reduce the environmental impact of effluents.

putida BS3701 attacked the oil globules from the outside (Fig. 4a), whereas Rhodococcus sp. S67 penetrated inside the oil globules (Fig. 4b). Irrespective of their locations, check details these bacteria, both in pure and mixed culture, secreted large amounts of polysaccharide materials in the form of films and granules (Fig. 4c), which were assessed by electron microscopic examinations of ultrathin sections stained with ruthenium red (Fig. 4d). Cytochemical staining with diaminobenzidine showed that oxidative

enzymes were located in the cell walls of both bacteria as well as in the extracellular films that were evenly distributed over the cell surfaces (Fig. 4e and f). The exocellular substances were most abundant when bacteria were cultivated in a mixed culture. Moreover, the mixed bacterial culture showed a greater efficiency in oil degradation in water medium than the individual bacteria (more than 70% in mixed cultures as compared with 50–60% observed for P. putida BS3701 and Rhodococcus sp. S67 as pure cultures). A 3D reconstruction of bacterial consortia grown on oil

(Fig. 5a and b) was performed to answer the questions: (1) Is there any expediency in the abundant release of polymer substances by microorganisms grown on oil hydrocarbons? (2) Do cells form any specific structures that facilitate the use of potential growth substrates contained in oil? To understand the structural behavior of microorganisms, a bacterial consortium containing

cells of Rhodococcus sp. S67 and P. putida was used as a model. The consortium Gemcitabine was grown in shaking flasks with crude oil as a sole carbon source. A visual analysis of the 3D features of bacterial structures formed in the oil demonstrated that the bacteria inhabited discrete cavities in the oil droplets that constituted a kind of ‘trophic’ vesicle or granule. All of the granules were bound to one another by polymer films and all of the unified structures comprised a well-developed network over the surface of the oil globules. Granules in the globules were either closed or open to the aqueous medium. Open granules probably served Fossariinae as emulsion traps for metabolites generated by oil degradation. The analysis of serial sections showed that after complete utilization of the substrate, the trophic units, or ‘trophosomes,’ broke down and the entire process of the substrate utilization involved a continuous assembly and decay of functional units in the network of exocellular granule vesicles. The present study reveals a possibly common scenario by which different yeasts and bacteria may colonize and utilize hydrophobic substrates as oil and its components (specifically n-alkanes) when suspended as droplets in an aqueous medium. The most notable feature for several of the yeasts studied here was the substrate-induced formation of ‘canals’ that permeated the cell walls and that were lined with exopolymers and oxidative enzymes.

putida BS3701 attacked the oil globules from the outside (Fig. 4a), whereas Rhodococcus sp. S67 penetrated inside the oil globules (Fig. 4b). Irrespective of their locations, MDV3100 purchase these bacteria, both in pure and mixed culture, secreted large amounts of polysaccharide materials in the form of films and granules (Fig. 4c), which were assessed by electron microscopic examinations of ultrathin sections stained with ruthenium red (Fig. 4d). Cytochemical staining with diaminobenzidine showed that oxidative

enzymes were located in the cell walls of both bacteria as well as in the extracellular films that were evenly distributed over the cell surfaces (Fig. 4e and f). The exocellular substances were most abundant when bacteria were cultivated in a mixed culture. Moreover, the mixed bacterial culture showed a greater efficiency in oil degradation in water medium than the individual bacteria (more than 70% in mixed cultures as compared with 50–60% observed for P. putida BS3701 and Rhodococcus sp. S67 as pure cultures). A 3D reconstruction of bacterial consortia grown on oil

(Fig. 5a and b) was performed to answer the questions: (1) Is there any expediency in the abundant release of polymer substances by microorganisms grown on oil hydrocarbons? (2) Do cells form any specific structures that facilitate the use of potential growth substrates contained in oil? To understand the structural behavior of microorganisms, a bacterial consortium containing

cells of Rhodococcus sp. S67 and P. putida was used as a model. The consortium ABT-199 cost was grown in shaking flasks with crude oil as a sole carbon source. A visual analysis of the 3D features of bacterial structures formed in the oil demonstrated that the bacteria inhabited discrete cavities in the oil droplets that constituted a kind of ‘trophic’ vesicle or granule. All of the granules were bound to one another by polymer films and all of the unified structures comprised a well-developed network over the surface of the oil globules. Granules in the globules were either closed or open to the aqueous medium. Open granules probably served PJ34 HCl as emulsion traps for metabolites generated by oil degradation. The analysis of serial sections showed that after complete utilization of the substrate, the trophic units, or ‘trophosomes,’ broke down and the entire process of the substrate utilization involved a continuous assembly and decay of functional units in the network of exocellular granule vesicles. The present study reveals a possibly common scenario by which different yeasts and bacteria may colonize and utilize hydrophobic substrates as oil and its components (specifically n-alkanes) when suspended as droplets in an aqueous medium. The most notable feature for several of the yeasts studied here was the substrate-induced formation of ‘canals’ that permeated the cell walls and that were lined with exopolymers and oxidative enzymes.