- Volume 153, Issue 5, 2007
Volume 153, Issue 5, 2007
- Environmental Microbiology
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Stabilization of water/gas oil emulsions by desulfurizing cells of Gordonia alkanivorans RIPI90A
More LessIt has been previously reported that resting-cells, non-proliferating cells, of Gordonia alkanivorans RIPI90A can convert dibenzothiophene (DBT) to 2-hydroxybiphenyl (2-HBP) via the 4S pathway in a biphasic system. The main goal of the current work was to study the behaviour of resting-cells of this strain in biphasic organic media. Resting-cells showed strong affinity for sulfurous organic substrates and were able to stabilize water/gas oil emulsions by attaching to the interface without decreasing the surface tension of their environment. This was consistent with the behaviour of the whole cells but not the surfactants, suggesting that microbial cell-mediated emulsification occurs. It was found that the emulsion-stabilizing activity of the resting-cells was influenced by the growth stage, but was not directly influenced by the metabolic activity of the resting-cells. This activity may be related to cell-surface hydrophobicity, which results from the unique chemical structure of the cell surface. In some biphasic biodesulfurization (BDS) bioreactors, emulsions are created without addition of any surfactant. Cell surface-mediated stabilization helps prolong the emulsions and therefore overcomes mass-transfer limitations in bioreactors. The simultaneous occurrence of emulsion-stabilizing and desulfurization activities of resting-cells was observed for what is believed to be the first time. The results suggest that this strain may have potential for the BDS of diesel oils.
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- Genes And Genomes
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Sequence analysis of the mobilizable lactococcal plasmid pGdh442 encoding glutamate dehydrogenase activity
More LessA novel plasmid named pGdh442 had previously been isolated from a plant Lactococcus lactis strain. This plasmid encodes two interesting properties with applications in the dairy industry: a glutamate dehydrogenase activity that stimulates amino acid conversion to aroma compounds, and cadmium/zinc resistance that can be used as a selectable marker. Moreover, this plasmid can be transferred naturally to other strains, but appears to be incompatible with certain other lactococcal plasmids. During this study, the complete sequence of pGdh442 (68 319 bp) was determined and analysed. This plasmid contains 67 ORFs that include 20 IS elements that may have mediated transfer events between L. lactis and other genera living in the same biotope, such as Streptococcus, Pediococcus and Lactobacillus. Even though it is a low-copy-number plasmid, it is relatively stable due to a theta replication mode and the presence of two genes involved in its maintenance system. However, pGdh442 is incompatible with pSK08-derived protease/lactose plasmids because both possess the same replication and partition system. pGdh442 is not self-transmissible, but can be naturally transmitted via mobilization by conjugative elements carried by the chromosome or by other plasmids, such as the 712-type sex factor, which is widely distributed in L. lactis. In addition to several genes already found on other L. lactis plasmids, such as the oligopeptide transport and utilization genes, pGdh442 also carries several genes not yet identified in L. lactis. Finally, it does not carry genes that would trigger concern over its presence in human food.
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- Pathogens And Pathogenicity
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Differential gene expression profiling of Streptococcus mutans cultured under biofilm and planktonic conditions
More LessStreptococcus mutans often adopts a sessile biofilm lifestyle that differs greatly from that of free-living cells. Biofilm formation represents a protected mode of growth that allows cells to survive in hostile environments. In this study, in vitro comparative transcriptome analysis was carried out to identify genes that are differentially expressed in biofilm of S. mutans compared with free-living cells. DNA-microarray analyses indicated that about 12 % of genes showed significant differential expression: 139 were activated and 104 were repressed in biofilm vs the planktonic environment. The differential expression of 20 selected genes was confirmed by real-time RT-PCR. In addition, regulation of expression of these genes during biofilm development was tested in 100 and 400 μm deep biofilms. Direct comparison of optical images consistently demonstrated that changes in biofilm thickness are accompanied by significant shifts in cell viability. From evaluation of gene expression patterns, it was shown that the majority of the genes tested were significantly down-regulated in 400 vs 100 μm deep biofilms. This study provides a genome-scale synopsis and adds important insights into gene expression in biofilm development processes of S. mutans, which are strongly associated with the pathogenesis of dental diseases.
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Effects of iron on DNA release and biofilm development by Pseudomonas aeruginosa
Extracellular DNA is one of the major matrix components in Pseudomonas aeruginosa biofilms. It functions as an intercellular connector and plays a role in stabilization of the biofilms. Evidence that DNA release in P. aeruginosa PAO1 biofilms is controlled by the las-rhl and pqs quorum-sensing systems has been previously presented. This paper provides evidence that DNA release in P. aeruginosa PAO1 biofilms is also under iron regulation. Experiments involving cultivation of P. aeruginosa in microtitre trays suggested that pqs expression, DNA release and biofilm formation were favoured in media with low iron concentrations (5 μM FeCl3), and decreased with increasing iron concentrations. Experiments involving cultivation of P. aeruginosa in a flow-chamber system suggested that a high level of iron (100 μM FeCl3) in the medium suppressed DNA release, structural biofilm development, and the development of subpopulations with increased tolerance toward antimicrobial compounds. Experiments with P. aeruginosa strains harbouring fluorescent reporters suggested that expression of the pqs operon was induced in particular subpopulations of the biofilm cells under low-iron conditions (1 μM FeCl3), but repressed in the biofilm cells under high-iron conditions (100 μM FeCl3).
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Rapid necrotic killing of polymorphonuclear leukocytes is caused by quorum-sensing-controlled production of rhamnolipid by Pseudomonas aeruginosa
Quorum sensing (QS) denotes a density-dependent mode of inter-bacterial communication based on signal transmitter molecules. Active QS is present during chronic infections with the opportunistic pathogen Pseudomonas aeruginosa in immunocompromised patients. The authors have previously demonstrated a QS-regulated tolerance of biofilm bacteria to the antimicrobial properties of polymorphonuclear leukocytes (PMNs). The precise QS-regulated effect on the PMNs is, however, unknown. Incubation of human PMNs with supernatants from dense P. aeruginosa cultures showed that the QS-competent P. aeruginosa induced rapid necrosis of the PMNs. This mechanism was also observed in mouse lungs infected with P. aeruginosa, and in sputum obtained from P.-aeruginosa-infected patients with cystic fibrosis. Evidence is presented that the necrotic effect was caused by rhamnolipids, production of which is QS controlled. The results demonstrate the potential of the QS system to facilitate infections with P. aeruginosa by disabling the PMNs, which are a major first line of defence of the host. Furthermore, the study emphasizes the inhibition of QS as a target for the treatment of infections with P. aeruginosa.
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An aflagellate mutant Yersinia enterocolitica biotype 1A strain displays altered invasion of epithelial cells, persistence in macrophages, and cytokine secretion profiles in vitro
More LessDespite being classically defined as non-pathogenic, there is growing evidence that biotype 1A Yersinia enterocolitica isolates may be aetiological agents of disease in humans. In previous studies, a potential link between motility and the ability of biotype 1A strains to invade cultured epithelial cells was observed. In an attempt to further investigate this finding, a flagella mutant was constructed in a human faecal Y. enterocolitica biotype 1A isolate. The flagella mutation abolished the ability of the strain to invade cultured human epithelial cells, although adherence was not affected. The aflagellate mutant was also attenuated in its ability to survive within cultured macrophages, being cleared after 3 h, whilst the wild-type persisted for 24 h after infection. Examination of cytokine secretion by infected macrophages also suggested that the flagella of biotype 1A strains act as anti-inflammatory agents, decreasing production of tumour necrosis factor (TNF)-α whilst increasing secretion of interleukin (IL)-10. Preliminary studies using porcine in vitro organ culture (IVOC) tissue suggested that the flagella mutant was also attenuated in its ability to colonize intestinal tissue.
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Analysis of the expression, regulation and export of NleA–E in Escherichia coli O157 : H7
Previous work has shown that locus of enterocyte effacement (LEE)-encoded effector proteins such as Tir and Map can be exported via the type III secretion system (T3SS) of Escherichia coli O157 : H7. Additionally, a family of non-LEE-encoded (Nle) effector proteins has been shown to be secreted from Citrobacter rodentium, homologues of which are located on the E. coli O157 chromosome. While NleA has been shown to be secreted from pathogenic E. coli, the secretion of other Nle effector proteins has only been detected under induced conditions, or using a mutated T3SS. This study aimed to determine: (1) which nle genes are expressed in E. coli O157 : H7 under secretion-permissive conditions; (2) if Nle proteins are secreted from wild-type E. coli O157 : H7 under secretion-permissive conditions; and (3) if nle gene expression is regulated co-ordinately with other LEE-encoded effectors. Using data generated from a combination of transcriptome arrays, reporter fusions and proteomics, it was demonstrated that only nleA is expressed co-ordinately with the LEE. Secretion and expression of NleA were regulated directly or indirectly by ler, a key activator of the LEE. MS confirmed the secretion of NleA into the culture supernatant, while NleB–F were not detected.
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Regulated synthesis of the Borrelia burgdorferi inner-membrane lipoprotein IpLA7 (P22, P22-A) during the Lyme disease spirochaete's mammal–tick infectious cycle
Results of previous immunological studies suggested that Borrelia burgdorferi regulates synthesis of the IpLA7 lipoprotein during mammalian infection. Through combined use of quantitative reverse transcription PCR, immunofluorescence analyses, ELISA and immunoblotting, it is now demonstrated that IpLA7 is actually expressed throughout mammalian infection, as well as during transmission both from feeding ticks to naïve mice and from infected mice to naïve, feeding ticks. However, proportions of IpLA7-expressing B. burgdorferi within tick midguts declined significantly with time following completion of blood feeding. Cultured bacteria differentially expressed IpLA7 in response to changes in temperature, pH and concentration of 4,5-dihydroxy-2,3-pentanedione, the precursor of autoinducer 2, indicative of mechanisms governing IpLA7 expression. Previous studies also reported mixed results as to the cellular localization of IpLA7. It is now demonstrated that IpLA7 localizes primarily to the borrelial inner membrane and is not surface-exposed, consistent with the ability of these bacteria to produce IpLA7 throughout mammalian infection despite being the target of a robust immune response.
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Disruption of the Candida albicans ATC1 gene encoding a cell-linked acid trehalase decreases hypha formation and infectivity without affecting resistance to oxidative stress
In Candida albicans, the ATC1 gene, encoding a cell wall-associated acid trehalase, has been considered as a potentially interesting target in the search for new antifungal compounds. A phenotypic characterization of the double disruptant atc1Δ/atc1Δ mutant showed that it was unable to grow on exogenous trehalose as sole carbon source. Unlike actively growing cells from the parental strain (CAI4), the atc1Δ null mutant displayed higher resistance to environmental insults, such as heat shock (42 °C) or saline exposure (0.5 M NaCl), and to both mild and severe oxidative stress (5 and 50 mM H2O2), which are relevant during in vivo infections. Parallel measurements of intracellular trehalose and trehalose-metabolizing enzymes revealed that significant amounts of the disaccharide were stored in response to thermal and oxidative challenge in the two cell types. The antioxidant activities of catalase and glutathione reductase were triggered by moderate oxidative exposure (5 mM H2O2), whereas superoxide dismutase was inhibited dramatically by H2O2, where a more marked decrease was observed in atc1Δ cells. In turn, the atc1Δ mutant exhibited a decreased capacity of hypha and pseudohypha formation tested in different media. Finally, the homozygous null mutant in a mouse model of systemic candidiasis displayed strongly reduced pathogenicity compared with parental or heterozygous strains. These results suggest not only a novel role for the ATC1 gene in dimorphism and infectivity, but also that an interconnection between stress resistance, dimorphic conversion and virulence in C. albicans may be reconsidered. They also support the hypothesis that Atc1p is not involved in the physiological hydrolysis of endogenous trehalose.
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Lipid composition and transcriptional response of Mycobacterium tuberculosis grown under iron-limitation in continuous culture: identification of a novel wax ester
The low level of available iron in vivo is a major obstacle for microbial pathogens and is a stimulus for the expression of virulence genes. In this study, Mycobacterium tuberculosis H37Rv was grown aerobically in the presence of limited iron availability in chemostat culture to determine the physiological response of the organism to iron-limitation. A previously unidentified wax ester accumulated under iron-limited growth, and changes in the abundance of triacylglycerol and menaquinone were also observed between iron-replete and iron-limited chemostat cultures. DNA microarray analysis revealed differential expression of genes involved in glycerolipid metabolism and isoprenoid quinone biosynthesis, providing some insight into the underlying genetic changes that correlate with cell-wall lipid profiles of M. tuberculosis growing in an iron-limited environment.
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Biological cost of hypermutation in Pseudomonas aeruginosa strains from patients with cystic fibrosis
The high prevalence of hypermutable (mismatch repair-deficient) Pseudomonas aeruginosa strains in patients with cystic fibrosis (CF) is thought to be driven by their co-selection with adaptive mutations required for long-term persistence. Whether the increased mutation rate of naturally hypermutable strains is associated with a biological benefit or cost for the colonization of secondary environments is not known. Thirty-nine P. aeruginosa strains were collected from ten patients with CF during their course of chronic lung infections and screened for hypermutability. Seven hypermutable P. aeruginosa strains (18 %) isolated from six patients with CF (60 %) were identified and assigned to five different genotypes. Complementation and sequence analysis in the mutS, mutL and uvrD genes of these hypermutable P. aeruginosa strains revealed novel mutations. To understand the consequences of hypermutation for the fitness of the organisms, five pairs of clinical wild-type/hypermutable, clonally related P. aeruginosa strains and the laboratory strains PAO1/PAO1ΔmutS were subjected to competition in vitro and in the agar-beads mouse model of chronic airway infection. When tested in competition assay in vitro, the wild-type outcompeted four clinical hypermutable strains and the PAO1ΔmutS strain. In vivo, all of the hypermutable strains were less efficient at establishing lung infection than their wild-type clones. These results suggest that P. aeruginosa hypermutation is associated with a biological cost, reducing the potential for colonization of new environments and therefore strain transmissibility.
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The Mycoplasma gallisepticum OsmC-like protein MG1142 resides on the cell surface and binds heparin
More LessMycoplasma gallisepticum is an avian pathogen that causes a chronic respiratory disease of chickens and results in significant economic losses to the poultry industry worldwide. Colonization of the host and the establishment of chronic disease are initiated by the cytadherence of M. gallisepticum to the host respiratory epithelium. While several proteins involved in cytadhesion have been characterized, molecules that interact with components of the host extracellular matrix, a process that is central to pathogenesis, are only now being identified. In this study, M. gallisepticum whole cells were shown to bind heparin in a specific and saturable manner. Heparin also significantly inhibited the binding of M. gallisepticum to the human lung fibroblast cell line MRC-5, suggesting a potential role for glycosaminoglycans (GAGs) in cytadherence. M. gallisepticum protein MG1142 (encoded by mga_1142), which displays homology to the osmotically induced (OsmC) family of proteins, binds strongly to heparin, is highly expressed during in vitro culture, and is surface accessible. Recombinant MG1142 bound heparin in a dose-dependent and saturable manner with a dissociation constant (K d) of 10±1.8 nM, which is within a physiologically significant range, compared to that of other heparin-binding proteins. Binding to heparin was inhibited by the heavily sulfated polysaccharide fucoidan, but not by mucin or chondroitin sulfate A or B, suggesting that electrostatic interactions between the sulfate groups of heparin and the positively charged basic residues of the MG1142 protein are important in binding. The ability of M. gallisepticum to bind GAGs may contribute to host adherence and colonization.
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Phenotypic characterization of a virulence-associated protein, VagH, of Yersinia pseudotuberculosis reveals a tight link between VagH and the type III secretion system
Recently, a number of attenuated mutants of Yersinia pseudotuberculosis have been identified using a bioinformatics approach. One of the target genes identified in that study was vagH, which the authors now characterized further. VagH shows homology to HemK of Escherichia coli, possessing methyltransferase activity similar to that of HemK, and targeting release factors 1 and 2. Microarray studies comparing the wild-type and the vagH mutant revealed that the mRNA levels of only a few genes were altered in the mutant. By proteome analysis, expression of the virulence determinant YopD was found to be increased, indicating a possible connection between VagH and the virulence plasmid-encoded type III secretion system (T3SS). Further analysis showed that Yop expression and secretion were repressed in a vagH mutant. This phenotype could be suppressed by trans-complementation with the wild-type vagH gene or by deletion of the negative regulator yopD. Also, in a similar manner to a T3SS-negative mutant, the avirulent vagH mutant was rapidly cleared from Peyer's patches and could not reach the spleen after oral infection of mice. In a manner analogous to that of T3SS mutants, the vagH mutant could not block phagocytosis by macrophages. However, a vagH mutant showed no defects in the T3SS-independent ability to proliferate intracellularly and replicated to levels similar to those of the wild-type in macrophages. In conclusion, the vagH mutant exhibits a virulence phenotype similar to that of a T3SS-negative mutant, indicating a tight link between VagH and type III secretion in Y. pseudotuberculosis.
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The outer membrane secretin PilQ from Neisseria meningitidis binds DNA
Neisseria meningitidis is naturally competent for transformation throughout its growth cycle. Transformation in neisserial species is coupled to the expression of type IV pili, which are present on the cell surface as bundled filamentous appendages, and are assembled, extruded and retracted by the pilus biogenesis components. During the initial phase of the transformation process, binding and uptake of DNA takes place with entry through a presumed outer-membrane channel into the periplasm. This study showed that DNA associates only weakly with purified pili, but binds significantly to the PilQ complex isolated directly from meningococcal membranes. By assessing the DNA-binding activity of the native complex PilQ, as well as recombinant truncated PilQ monomers, it was shown that the N-terminal region of PilQ is involved in the interaction with DNA. It was evident that the binding of ssDNA to PilQ had a higher affinity than the binding of dsDNA. The binding of DNA to PilQ did not, however, depend on the presence of the neisserial DNA-uptake sequence. It is suggested that transforming DNA is introduced into the cell through the outer-membrane channel formed by the PilQ complex, and that DNA uptake occurs by non-specific introduction of DNA coupled to pilus retraction, followed by presentation to DNA-binding component(s), including PilQ.
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svrA, a multi-drug exporter, does not control agr
More LessThe Staphylococcus aureus svrA gene was identified in a signature-tagged mutagenesis screen for Tn917 insertions attenuated for mouse virulence, and subsequently found to be defective in agr expression. Its attenuation of virulence was attributed to its failure to express the agr regulon. In addition to the Tn917 insertion in svrA, the original svrA mutant strain (P6C63) has an adventitious frame-shift in agrC, which results in truncation of the AgrC peptide. Separation of the svrA mutation from the agrC frame-shift revealed that svrA has no detectable affect on agr activation, as assessed by exoprotein profiles and the production of haemolytic toxins. These results indicate that svrA does not play a role in Staphylococcus aureus infections via an agr-mediated pathway.
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Identification of new genes associated with intermediate resistance of Enterococcus faecalis to divercin V41, a pediocin-like bacteriocin
More LessIt has been suggested that resistance to class IIa bacteriocins occurs at either a low or a high level. In listerial strains, low-level resistance (2–4-fold) to class IIa bacteriocins is attributed to alterations in membrane lipid composition. In Listeria monocytogenes and Enterococcus faecalis, high-level resistance (1000-fold) correlates with inactivation of the mptACD operon, which encodes the EIIMan t mannose permease of the phosphotransferase system (PTS). Previous studies reported that in L. monocytogenes, high-level resistance involved the σ 54 factor and the ManR activator. In this investigation, three genes associated with the resistance of Ent. faecalis JH2-2 to divercin V41, a pediocin-like bacteriocin from Carnobacterium divergens V41, were clearly identified by screening an insertional mutant library of Ent. faecalis JH2-2. These genes correspond to the well-known rpoN gene, which encodes σ 54 factor, and to genes encoding a glycerophosphoryl diester phosphodiesterase (GlpQ) and a protein with a putative phosphodiesterase function (PDE). Resistance of the three mutants defective in the aforementioned genes appeared to be graduated: the rpoN mutant was more resistant than the glpQ mutant, which was more resistant than the pde mutant. Moreover, this resistance was specific to class IIa bacteriocins.
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- Physiology
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The key role of the mycolic acid content in the functionality of the cell wall permeability barrier in Corynebacterineae
Recently, it has been shown that trehalose and mycolic acids are essential for the growth of Mycobacterium tuberculosis, the causative agent of tuberculosis, and Mycobacterium smegmatis, and important but not indispensable to the survival of Corynebacterium glutamicum. Therefore, to investigate the function of mycolic acids in both the permeability of the cell wall to small nutrients and antibiotics, and the excretion of amino acids by C. glutamicum, a trehalose-deficient mutant of the l-lysine producer ATCC 21527, designated LPΔtreSΔotsAΔtreY, was constructed. By using different carbon sources in either the presence or the absence of external trehalose, a set of endogenously trehalose-free LPΔtreSΔotsAΔtreY cells that exhibited various mycolate contents was generated. The results showed that the structure of the arabinogalactan of these different cell types of LPΔtreSΔotsAΔtreY was not affected when the mycolic acid layer was either missing or impaired. Nevertheless, cells were more susceptible to antibiotics, and the permeability of their cell walls to glycerol was increased. Interestingly, a concomitant increase in the excretion of both l-lysine and l-glutamate was also observed, indicating that the mycolic acid content of the permeability barrier (and not only the peptidoglycan and/or the arabinogalactan) is implicated in the glutamate excretion process.
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Turgor regulation in the osmosensitive cut mutant of Neurospora crassa
More LessThe internal hydrostatic pressure (turgor) of fungal cells is maintained at 400–500 kPa. The turgor is regulated by changes in ion flux and by production of the osmotically active metabolite glycerol. In Neurospora crassa, there are at least two genetically distinct pathways that function in adaptation to hyperosmotic shock. One involves a mitogen-activated protein (MAP) kinase cascade (kinases OS-4, OS-5 and OS-2 downstream of the osmosensing OS-1); the other is less understood, but involves the cut gene, which encodes a putative phosphatase. This study examined turgor regulation, electrical responses, ion fluxes and glycerol accumulation in the cut mutant. Turgor recovery after hyperosmotic treatment was similar to that in the wild-type, for both time-course (∼40 min) and magnitude. Prior to turgor recovery, the hyperosmotic shock caused a rapid transient depolarization of the membrane potential, followed by a sustained hyperpolarization that occurred concomitant with increased H+ efflux, indicating that the plasma membrane H+-ATPase was being activated. These changes also occurred in the wild-type. Net fluxes of Ca2+ and Cl− during turgor recovery were similar to those in the wild-type, but K+ influx was attenuated in the cut mutant. The similar turgor recovery can be explained by the ion uptake, since glycerol did not accumulate in the cut mutant within the time frame of turgor recovery (but did accumulate in the wild-type). The results suggest that turgor regulation involves multi-faceted coordination of both ion flux and glycerol accumulation. Ion uptake is activated by a MAP kinase cascade, while CUT is required for glycerol accumulation.
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Volumes and issues
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