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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cellular phenol-water extract of Acetobacter xylinum NRC 17007 was fractionated on Sepharose 4 B. The fraction eluting with the void volume consisted to about 95% of glycogen-like material. The lipopolysaccharide fraction was of lower molecular weight and had the following composition (%, w/w): Mannose, 42; glucose, 7; galactose, 3.8; heptose, 2; 2-keto-3-deoxy-octonate, 1.2; glucosamine, 3.3; phosphate, 4.5; total fatty acids, 3.9. Among the fatty acids, 3-hydroxy-tetradecanoic acid was present, and 2-hydroxy-hexadecanoic acid predominated.
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PMID:Isolation of alpha-glucan and lipopolysaccharide fractions from Acetobacter xylinum. 60 42

The lipopolysaccharide from Thiocapsa roseopersicina was isolated by phenol/water, being found in the water phase. It is cleaved into a polysaccharide moiety (degraded polysaccharide) and lipid A by hydrolysis with 10% acetic acid (100 degree C, 3 h). D-Mannose, L-rhamnose, 3-amino-3, 6-dideoxy-D-galactose and D-glucose are the major constituents of the degraded polysaccharide. 2-O-Methyl-L-rhamnose, 3-O-methyl-D-mannose, D-galactose, glucosamine and quinovosamine are minor constituents. D-Glycer-D-manno-heptose (tentatively identified) and 3-deoxy-D-manno-octulosonic acid were detected in only small amounts. Conspicuously, lipid A from T. roseopersicina contains a neutral sugar, D-mannose, in addition to D-glucosamine, as had been observed with lipid A from Chromatium vinosum D. Major fatty acids are beta-hydroxymyristic and lauric acids. Only trace amounts of phosphorus were found indicating this lipid A to be free of phosphate. The lipopolysaccharide of T. roseopersicina represents the O-antigen of the strain. It reacts with antisera prepared against living or heat-killed cells in passive hemagglutination.
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PMID:Isolation and characterization of the lipopolysaccharide of Thiocapsa roseopersicina. 71 Apr 28

The composition of lipopolysaccharide and polysaccharides isolated after acidic or alkaline degradation of lipopolysaccharide of Salmonella toucra has been investigated. The following analytical methods were used in this study: gel-filtration and ion-exchange techniques, paper and gas-liquid chromatography as well as spectrophotometric analysis. The products of the lipopolysaccharide degradation were fractionated on the Sephadex G-25 and Sephadex G-50 columns. Lipopolysaccharide and products of its degradation besides glucosamine, galactose, glucose, heptose(s) and 3-deoxy-D-manno-octulosonate described as 'basal' sugars, also contained N-acetylneuraminic acid and an unidentified amino sugar.
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PMID:N-Acetylneuraminic acid: a constituent of the lipopolysaccharide of Salmonella toucra. 72 82

Chemical and serological investigations were carried out on lipopolysaccharides of 4 Salmonella S-forms and of 1 SR-mutant, extracted from bacteria at different ages of culture (early exponential to stationary growth phase). The results show that the fatty acid composition of Lipid A (lauric-, myristic-, palmitic-, and beta-hydroxy-myristic acids) does not undergo any significant change during the growth of the cultures. However, there are differences in the molar ratios of the fatty acids from strain to strain. In all phases of growth Lipid A is substituted by basaloligosaccharide, to the same extent, as can be seen from the constant ratios of beta-hydroxy-myristic acid: heptose. Serological experiments (haemagglutination inhibition tests, absorption of antibodies by LPS-coated erythrocytes) showed that in no case the basaloligosaccharide is completely substituted by O-specific chains and that basaloligosaccharide exhibits free R-antigen structures which are mainly of chemotypes Ra, Rb and Rc, for the SR-mutant only of types Ra and Rb. There is no demonstrable dependence upon the phases of growth. In the O-specific polysaccharide chains the sugars of the main chain and the side bound dideoxy sugars (abequose and tyvelose) show a constant 1:1 molar ratio in all phases. In the case of S. typhimurium, antigen factors 1, 4 and 12(2), the biosynthesis of which is controlled by modifying oaf genes and/or by a lysogenic phage, are of a somewhat weaker expression in the exponential phase than in the latter phases of growth. In the SR-mutant, lipopolysaccarides with (low) serological O1 and O12(2) activity are only extractable by the phenol/water method, but not by the PCP method. In three out of four S-forms, changes occur in the length of the O-specific polysaccharide chains, whereas the number of repeating units of the fourth strain remains almost unchanged. The lipopolysaccharides of the SR-mutant contain in all phases of growth about one repeating unit. In all strains the covering of the cell surface by lipopolysaccharide molecules changes during the course of growth, as can be seen by comparing the relative cell surface and the content of Lipid A fatty acids of the bacteria. Lipid A synthesis in the 4 S-forms is reduced in the exponential phase and/or in the phase of delayed growth acceleration. The extent of biosynthesis of the carbohydrate moiety of lipopolysaccharides is independent of that of Lipoid A. In the SR-mutant, Lipoid A and Polysaccharide are formed in increased amounts in the exponential growth phase.
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PMID:[Chemical and serological characterization of Salmonella lipopolysaccharides from different phases of growth (author's transl)]. 76 1

The structure of the lipopolysaccharide from Escherichia coli K12, strain CR34 has been investigated. The lipopolysaccharide contains D-galactose, D-glucose, D-glucosamine, L-glycero D-mannoheptose, 2-keto-3-deoxyoctonate and lipid A. The core region does not contain D-glucosamine but contains galactose, glucose, and heptose in the molar ratios 1:3:6. Methylations were performed on the lipopolysaccharide and on the degraded polysaccharide obtained after acetic acid hydrolysis of the lipopolysaccharide. It was found that galactose is in terminal position partly in the form of galactopyranose, partly in the form of galactofuranose. A part of the heptose was found as unsubstituted heptofuranose. A mole of glucose was 1 leads to 2 linked and another mole of glucose was 1 leads to 6 linked. Periodate oxidation of the lipopolysaccharide followed by borohydride reduction eliminates galactose and only a part of glucose and of heptose. A mole of heptose gave mannose and thus it is unsubstituted in C6 and C7. One mole of glucose and one mole of heptose were not degraded by periodate oxidation.
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PMID:[Study of the lipopolysaccharide from Escherichia coli K12 CR34]. 77 Jan 68

Freeze etching showed that the loss of each of the major outer membrane proteins b, c or d in mutants of Escherichia coki K12 does not influence the morphology of fracture faces of the outer membrane. Mutants that possess a heptose-deficient lipopolysaccharide and which in addition are deficient in one or more major outer membrane proteins exhibit a reduction in the number of intramembranous particles of the outer membrane. Moreover it was shown that lipid phase transitions induce a lateral lipid protein separation in the outer membrane, similar to that found in the cytoplasmic membrane.
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PMID:Freeze etch morphology of outer membrane mutants of Escherichia coli K12. 77 30

Two F- mutants deficient in conjugation with F-type donors are isolated and characterized. Phenotypically, these mutants are similar; they have heptose-less lipopolysaccharide and lack some outer membrane protein. Genotypically, they are different. One mutant harbors a point mutation in the 70 to 74 min region, while the other is deleted for the chromosomal region 6.5 to 8.5 min. Comparison of the properties of the conjugation-deficient mutants described in this paper with other such mutants suggests that an outer membrane protein is the receptor for the f-pilus.
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PMID:Conjugation deficient E. coli K12 F- mutants with heptose-less lipopolysaccharide. 78 7

The virulence and antigenic characters of Salmonella typhimurium strains, identical except for known lipopolysaccharide core defects, were compared. Smooth strains multiplied extensively and killed most mice. Deep rough strains containing only heptose I or heptose I and II in the rough core were completely eliminated after 6 h, whereas more superficial rough strains containing additional core sugars could be detected in low numbers (10(4) colony-forming units/g of tissue) for at least 7 days postinjection. Normal human serum exhaustively absorbed with certain rough strains was tested for ability to kill other rough strains. Two strains with the most superficial defects (rfaJ, rfaL) each had a unique serological character; strains with deeper defects showed much cross-reactivity. Similarities between the susceptibility of strains to the bactericidal effect of specifically absorbed serum correlated, in some cases, with similarities in in vivo behavior.
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PMID:Characterization of the virulence and antigenic structure of Salmonella typhimurium strains with lipopolysaccharide core defects. 78 75

Mutants of Escherichia coli K12, deficient in up to three major outer membrane proteins b, c and d have been constructed. Mutants that lack the lipopolysaccharide sugar heptose are deficient in protein b. All heptose-deficient strains are supersensitive to lysozyme, various antibiotics and detergents. They excrete the periplasmic enzyme ribonuclease I. Mutants deficient in proteins c and/or d have the same sensitivity towards these compounds as the parent strain. Cells of single, double and triple mutants are all rod-shaped. Electrophoretic analysis of cell envelope proteins indicates that in some mutants the protein deficiency is partially compensated for by increased amounts of one or two of the other major outer membrane proteins. Heptose-deficient strains have an increased amount of 2-keto-3-deoxyoctonate.
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PMID:Heptose-deficient mutants of Escherichia coli K12 deficient in up to three major outer membrane proteins. 78 63

Smooth strains of Salmonella typhimurium and S. minnesota, and chemotypes Ra, Rb, and Rc, which are deficient in lipopolysaccharide components of the somatic side chains and outer core region, grow normally on nutrient agar and nutrient broth up to 45 degrees C. However, most mutants with defects in the heptose region of the LPS (chemotypes Rd2 and Re) do not grow on this medium at 42 degrees C or above; a few grow at 42 degrees C but not at 45 degrees C. In liquid medium (nutrient broth, or phosphate minimal medium), growth, measured as turbidity or as colony-forming units, stops 60 to 90 min after shift from 30 to 42 degrees C; DNA and protein synthesis cease at the same time. Growth does not reoccur at 42 degrees C; protein synthesis and growth reinitiate upon shift to 30 or 37 degrees C. Growth cessation does not alter cell morphology in the phase-contrast microscope. Growth of heptose-deficient strains at 42 degrees C in nutrient broth is restored by MgCl2 (0.5 mM), NaCl (50 mM), or sucrose (100 mM). Sensitivity to smooth-specific and rough-specific phages, and analysis of LPS composition, indicate that heptose-deficient mutants grown at temperatures from 30 to 45 degrees C, and in the presence or absence of high salt, do not contain heptose or O-specific sugars in their LPS.
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PMID:Influence of temperature on growth of lipopolysaccharide-deficient (rough) mutants of Salmonella typhimurium and Salmonella minnesota. 78 69


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