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A new structure of a lipid and its covalent linkage to a protein (murein-lipoprotein of the Escherichia coli outer membrane) is described. Glycerylcysteine (S-(propane-2',3'-diol)-3-thio2-aminopropanic acid) at the N-terminal end of the polypeptide chain is the attachment site of two ester-bound fatty acids. An additional fatty acid is bound as amide to the N-terminal group. The diglyceride residue on the cysteine could be derived from the phospholipid pathway since the fatty acid composition is very similar to that of the phospholipids from the same cells. In contrast, 65% of the amide-linked fatty acid is palmitate. The main fatty acids are palmitic acid (53%), cis-vaccenic acid (20.7%), 9,10-methylene-hexadecanoic acid (10.6%) and palmitoleic acid (9.4%). The structure of glycerylcysteine was established by chemical degradation of the compound containing the fatty acids, by incorporation studies of [35S]sulfate, [35S]cysteine, [14C]cystine, [methyl-³H]methionine and [2-³H]glycerol and by chemical synthesis. Glycerylcysteine was isolated as a constituent of the peptide (Ser)-Ser-Asn-Ala-Lys. The C-terminal part of the lipopeptide sequence overlaps with the N-terminal end of the known sequence of the polypeptide chain. Its N-terminal position was confirmed by isolation of the N-terminal polypeptide fragment (position 1-31) after cleavage with cyanogen bromide. This contained the lipid. [ABSTRACT FROM AUTHOR]

Aerobic bacteria were excluded as a major source of lipases when it was found, in a previous study, that their virtual eradication by topical neomycin did not lower the free fatty acids (FFA) in scalp lipids. We now report the reciprocal experiment in which an oral tetracycline was used to suppress the anaerobic organisms. Nine healthy adults received 600 mgm of demethylchlortetracycline (DMCT) daily for 6 weeks. During this time we followed the composition of scalp lipid by thin layer chromatography and the densities of C. acnes, aerobes and yeasts on scalp and forehead. Six subjects had high initial levels of C. acnes. In these the FFA fell from 43% to 23% with a more than 99% reduction in the density of C. acnes. In three who initially had insignificant quantities of C. acnes the FFA were at the start only 25% and did not decline with treatment. The density of the aerobic population was not affected by DMCT owing to development of resistance. Yeasts were also unaffected. The finding that the FFA were proportional to the level of C. acnes suggests that these organisms are the chief source of lipolytic enzymes. The FFA levels began to decline earlier than the density of C. acnes. This might be explained either by enzyme inhibition or by bacteriostatic effect. [ABSTRACT FROM AUTHOR]