The major structural component of bacterial cell walls, peptidoglycan (PG), is not a static macromolecule but it is being cleaved continuously by autolysins that create sites for the insertion of new PG precursors during cell growth and division. In view of their ability to cause cellular lysis if their activity is allowed to proceed unchecked, it is essential for viability that a bacterium has mechanisms in place to control its endogenous autolysins. These include the compartrnentalization and physical association of the enzymes, the production of specific proteinaceous inhibitors, and the chemical modification of the substrate. A relatively common form of chemical modification of the PG sacculus to control autolysin activity is O-acetylation.
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