LOCALIZED PERFORATION OF THE CELL-WALL BY A MAJOR AUTOLYSIN - ATL GENE-PRODUCTS AND THE ONSET OF PENICILLIN-INDUCED LYSIS OF STAPHYLOCOCCUS-AUREUS

We investigated the cell surface localization of the af2 gene products of Staphyloccocus aureus exposed to a lytic concentration (4 MIC) of penicillin G (PCG) by means of immunoelectron microscopy using anti-62 -kDa N-acetylmuramyl-L-alanine amidase or anti-51-kDa endo-beta-N-acet ylglucosaminidase immunoglobulin G. Protein A-gold conjugates reacting with antigen-antibody complex localized at sites of defects of the ce ll wall at the nascent cross wall. Anti-62-kDa N-acetylmuramyl-L-alani ne amidase or endo-beta-N-acetylglucosaminidase immunoglobulin G inhib ited the decreased turbidity caused by PCG-induced lysis and the forma tion of defects in the waif, The autolysis-defective mutant, S. aureus RUSAL2 (atl::Tn551), exposed to 4 MIC of PCG resisted autolysis and f ormation of the wall defect. These results suggest that activation or deregulation of the atl gene products at localized sires where formati on of new cross wall was disturbed by PCG causes small defects in the cell wall in situ, eventually leading to general autolysis.