Metabolism of p- and m-xylene by species of Pseudomonas

1968 ◽  
Vol 14 (9) ◽  
pp. 1005-1009 ◽  
Author(s):  
R. S. Davis ◽  
F. E. Hossler ◽  
R. W. Stone
Keyword(s):  
Carbon Source ◽  
Growth Medium ◽  
Oxidative Metabolism ◽  
Sole Carbon Source ◽  
Growth Media ◽  
Toluic Acids

Species of Pseudomonas isolated from soil could utilize m- or p-xylene as the sole carbon source. The respective toluic acids of the xylenes were isolated from growth media and from cells suspended in buffer. Cells grown on either hydrocarbon were capable of "meta" type cleavage of catechol and the methylcatechols. A compound whose properties were consistent with the structure of 2-hydroxy-5-methylmuconic semialdehyde was produced when cell-free extracts of p-xylene-grown cells were confronted with 4-methylcatechol. This muconic semialdehyde was present in the growth medium of p-xylene-grown cells and in buffer suspensions of these cells confronted with p-xylene. Paraxylene-grown cells oxidized p-chlorotoluene and 4-chloro-catechol to a compound with a spectrum similar to those of "meta" cleavage products. Chemical isolations and manometric data are consistent with a pathway for the oxidative metabolism of p-xylene which includes p-methylbenzyl alcohol, p-tolualdehyde, p-toluic acid, 4-methylcatechol, and 2-hydroxy-5-methylmuconic semialdehyde.

Cometabolic oxidation of phenanthrene to phenanthrenetrans-9,10-dihydrodiol byMycobacteriumstrain S1 growing on anthracene in the presence of phenanthrene

1999 ◽  
Vol 45 (5) ◽  
pp. 369-376 ◽  
Author(s):  
Saowanit Tongpim ◽  
Michael A Pickard
Keyword(s):  
Carbon Source ◽  
Growth Medium ◽  
Aromatic Compounds ◽  
Sole Carbon Source ◽  
Polycyclic Aromatic Compounds ◽  
P450 Monooxygenase ◽  
Original Source ◽  
Dead End ◽  
Polycyclic Aromatic ◽  
Rhodococcus Strain

Mycobacterium strain S1, originally described as Rhodococcus strain S1 by chemotaxonomic criteria, was isolated by growth on anthracene, and is unable to use any of nine other polycyclic aromatic compounds as carbon source. Metabolism of phenanthrene during growth on anthracene as sole carbon source results in the accumulation of traces of a dihydrodiol metabolite in the growth medium, which, by comparison with authentic standards, has been tentatively identified as phenanthrene trans-9,10-dihydrodiol. Anthracene metabolites were ruled out on the basis of comparisons with authentic anthracene dihydrodiols from Pseudomonas fluorescens D1 and chemically synthesized anthrols. The original source of phenanthrene for dihydrodiol production was phenanthrene present as a <1% contaminant in the anthracene used as carbon source. However, addition of further phenanthrene to the anthracene growth medium increased the level of phenanthrene trans-9,10-dihydrodiol formed. Mycobacterium strain S1 also produced phenanthrene trans-9,10-dihydrodiol when grown in a glucose-salts medium in the presence of phenanthrene. This dihydrodiol is a dead-end metabolite, and neither it nor its parent hydrocarbon are able to support the growth of Mycobacterium strain S1. Studies with metyrapone and ancimidol, which did not inhibit growth on anthracene but did inhibit formation of phenanthrene trans-9,10-dihydrodiol, suggest it is likely the product of a cytochrome P450 monooxygenase-like activity.Key words: phenanthrene trans-9,10-dihydrodiol, Mycobacterium.

Cholesterol is accumulated by mycobacteria but its degradation is limited to non-pathogenic fast-growing mycobacteria

2000 ◽  
Vol 46 (9) ◽  
pp. 826-831 ◽  
Author(s):  
Yossef Av-Gay ◽  
Rafat Sobouti
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Carbon Source ◽  
Sole Carbon Source ◽  
Mycobacterial Infection ◽  
Growth Media ◽  
Bacillus Calmette Guerin ◽  
Liquid Media ◽  
Fast Growing ◽  
Solid Media ◽  
Slow Growing

In this report we show that fast-growing non-pathogenic mycobacteria degrade cholesterol from liquid media, and are able to grow on cholesterol as a sole carbon source. In contrast, slow-growing mycobacteria, including pathogenic Mycobacterium tuberculosis and bacillus Calmette-Guérin (BCG), do not degrade and use cholesterol as a carbon source. Nevertheless, pathogenic mycobacteria are able to uptake, modify, and accumulate cholesterol from liquid growth media, and form a zone of clearance around a colony when plated on solid media containing cholesterol. These data suggest that cholesterol may have a role in mycobacterial infection other than its use as carbon source.Key words: mycobacteria, cholesterol, biodegradation.

scholarly journals Defects in Galactose Metabolism and Glycoconjugate Biosynthesis in a UDP-Glucose Pyrophosphorylase-Deficient Cell Line Are Reversed by Adding Galactose to the Growth Medium

2020 ◽  
Vol 21 (6) ◽  
pp. 2028
Author(s):  
Christelle Durrant ◽  
Jana I. Fuehring ◽  
Alexandra Willemetz ◽  
Dominique Chrétien ◽  
Giusy Sala ◽  
...  
Keyword(s):  
Carbon Source ◽  
Cell Line ◽  
Growth Medium ◽  
Sole Carbon Source ◽  
Chinese Hamster ◽  
Lung Fibroblasts ◽  
Wild Type ◽  
Galactose Metabolism ◽  
Partial Restoration ◽  
Fold Reduction

UDP-glucose (UDP-Glc) is synthesized by UGP2-encoded UDP-Glc pyrophosphorylase (UGP) and is required for glycoconjugate biosynthesis and galactose metabolism because it is a uridyl donor for galactose-1-P (Gal1P) uridyltransferase. Chinese hamster lung fibroblasts harboring a hypomrphic UGP(G116D) variant display reduced UDP-Glc levels and cannot grow if galactose is the sole carbon source. Here, these cells were cultivated with glucose in either the absence or presence of galactose in order to investigate glycoconjugate biosynthesis and galactose metabolism. The UGP-deficient cells display < 5% control levels of UDP-Glc/UDP-Gal and > 100-fold reduction of [6-3H]galactose incorporation into UDP-[6-3H]galactose, as well as multiple deficits in glycoconjugate biosynthesis. Cultivation of these cells in the presence of galactose leads to partial restoration of UDP-Glc levels, galactose metabolism and glycoconjugate biosynthesis. The Vmax for recombinant human UGP(G116D) with Glc1P is 2000-fold less than that of the wild-type protein, and UGP(G116D) displayed a mildly elevated Km for Glc1P, but no activity of the mutant enzyme towards Gal1P was detectable. To conclude, although the mechanism behind UDP-Glc/Gal production in the UGP-deficient cells remains to be determined, the capacity of this cell line to change its glycosylation status as a function of extracellular galactose makes it a useful, reversible model with which to study different aspects of galactose metabolism and glycoconjugate biosynthesis.

scholarly journals Pandrug-resistant Pseudomonas sp. expresses New Delhi metallo-β-lactamase-1 and consumes ampicillin as sole carbon source

2020 ◽  
Author(s):  
Vivek Kumar Ranjan ◽  
Shriparna Mukherjee ◽  
Subarna Thakur ◽  
Krutika Gupta ◽  
Ranadhir Chakraborty
Keyword(s):  
Carbon Source ◽  
Sole Carbon Source ◽  
New Delhi ◽  
Pseudomonas Sp

scholarly journals Study of a plugging microbial consortium using crude oil as sole carbon source

2008 ◽  
Vol 5 (4) ◽  
pp. 367-374 ◽  
Author(s):  
Jing Wang ◽  
Guiwen Yan ◽  
Mingquan An ◽  
Jieli Liu ◽  
Houming Zhang ◽  
...  
Keyword(s):  
Carbon Source ◽  
Crude Oil ◽  
Sole Carbon Source ◽  
Microbial Consortium

scholarly journals Mutants affecting histidine utilization inAspergillus nidulans

1975 ◽  
Vol 25 (2) ◽  
pp. 119-135 ◽  
Author(s):  
Meryl Polkinghorne ◽  
M. J. Hynes
Keyword(s):  
Carbon Source ◽  
Nitrogen Source ◽  
Sole Carbon Source ◽  
Nitrogen Sources ◽  
Limiting Factor ◽  
Sole Nitrogen Source ◽  
Wild Type ◽  
Exogenous Substrate ◽  
Growth Properties ◽  
Type Strains

SUMMARYWild-type strains ofAspergillus nidulansgrow poorly onL-histidine as a sole nitrogen source. The synthesis of the enzyme histidase (EC. 4.3.1.3) appears to be a limiting factor in the growth of the wild type, as strains carrying the mutantareA102 allele have elevated histidase levels and grow strongly on histidine as a sole nitrogen source.L-Histidine is an extremely weak sole carbon source for all strains.Ammonium repression has an important role in the regulation of histidase synthesis and the relief of ammonium repression is dependent on the availability of a good carbon source. The level of histidase synthesis does not respond to the addition of exogenous substrate.Mutants carrying lesions in thesarA orsarB loci (suppressor ofareA102) have been isolated. The growth properties of these mutants on histidine as a sole nitrogen source correlate with the levels of histidase synthesized. Mutation at thesarA andsarB loci also reduces the utilization of a number of other nitrogen sources. The data suggest that these two genes may code for regulatory products involved in nitrogen catabolism. No histidase structural gene mutants were identified and possible explanations of this are discussed.

Isolation of alcohol oxidase and two other methanol regulatable genes from the yeast Pichia pastoris

1985 ◽  
Vol 5 (5) ◽  
pp. 1111-1121
Author(s):  
S B Ellis ◽  
P F Brust ◽  
P J Koutz ◽  
A F Waters ◽  
M M Harpold ◽  
...  
Keyword(s):  
Pichia Pastoris ◽  
Carbon Source ◽  
Sole Carbon Source ◽  
Alcohol Oxidase ◽  
Methylotrophic Yeasts ◽  
Sequence Analyses ◽  
Yeast Pichia Pastoris ◽  
Oxidation Of Methanol ◽  
Regulated Expression

The oxidation of methanol follows a well-defined pathway and is similar for several methylotrophic yeasts. The use of methanol as the sole carbon source for the growth of Pichia pastoris stimulates the expression of a family of genes. Three methanol-responsive genes have been isolated; cDNA copies have been made from mRNAs of these genes, and the protein products from in vitro translations have been examined. The identification of alcohol oxidase as one of the cloned, methanol-regulated genes has been made by enzymatic, immunological, and sequence analyses. Methanol-regulated expression of each of these three isolated genes can be demonstrated to occur at the level of transcription. Finally, DNA subfragments of two of the methanol-responsive genomic clones from P. pastoris have been isolated and tentatively identified as containing the control regions involved in methanol regulation.

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