[PDF][PDF] Changes in the chemical structure of walls of Staphylococcus aureus grown in the presence of chloramphenicol

L Johannsen, H Labischinski, B Reinicke… - FEMS Microbiology …, 1983 - Citeseer
L Johannsen, H Labischinski, B Reinicke, P Giesbrecht
FEMS Microbiology Letters, 1983Citeseer
The main skeletal component of nearly all bacterial cell walls is a unique polymer called
peptidoglycan. Its primary structure consists of polysaccharide chains which in turn are cross-
linked by peptide strands made up of alternating D-and L-amino acids [1, 2]. Peptidoglycan
is known to be a very stable structure which, therefore, has even been used as a taxonomic
marker; Schleifer et al. reported that also various exogenous and endogenous factors had
only negligible effects on the chemical composition of peptidoglycan [2, 3]. However, the …
The main skeletal component of nearly all bacterial cell walls is a unique polymer called peptidoglycan. Its primary structure consists of polysaccharide chains which in turn are cross-linked by peptide strands made up of alternating D-and L-amino acids [1, 2]. Peptidoglycan is known to be a very stable structure which, therefore, has even been used as a taxonomic marker; Schleifer et al. reported that also various exogenous and endogenous factors had only negligible effects on the chemical composition of peptidoglycan [2, 3]. However, the walls of cells grown under amino acid starvation or in the presence of bacteriostatic antibiotics such as chloramphenicol (CAP) are more resistant to lysozyme or autolytic enzymes [4, 5]. Since qualitative or quantitative alterations of the aut01ysins were not detected [4, 6] changes should take place either in the chemical composition of the peptidoglycan or in its complex three-dimensional structure [7-10] or in both which could explain the different behaviour of the cell-wall materials towards degradation.
In this paper we report that among all the chemical parameters investigated so far only the content of O-acetyl groups was changed and appeared to be significantly higher in walls of Staphylococcus aureus cells treated with chloramphenicol than in walls of untreated cells. This
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