Localized perforation of the cell wall by a major autolysin: atl gene products and the onset of penicillin-induced lysis of Staphylococcus aureus

被引:51
作者
Sugai, M
Yamada, S
Nakashima, S
Komatsuzawa, H
Matsumoto, A
Oshida, T
Suginaka, H
机构
[1] KAWASAKI MED SCH, DEPT MICROBIOL, OKAYAMA 70101, JAPAN
[2] TANABE SEIYAKU CO LTD, LEAD GENERAT RES LAB, TODA, SAITAMA 335, JAPAN
关键词
D O I
10.1128/jb.179.9.2958-2962.1997
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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-acetylglucosaminidase immunoglobulin G. Protein A-gold conjugates reacting with antigen-antibody complex localized at sites of defects of the cell wall at the nascent cross wall. Anti-62-kDa N-acetylmuramyl-L-alanine amidase or endo-beta-N-acetylglucosaminidase immunoglobulin G inhibited the decreased turbidity caused by PCG-induced lysis and the formation of defects in the waif, The autolysis-defective mutant, S. aureus RUSAL2 (atl::Tn551), exposed to 4 MIC of PCG resisted autolysis and formation of the wall defect. These results suggest that activation or deregulation of the atl gene products at localized sires where formation of new cross wall was disturbed by PCG causes small defects in the cell wall in situ, eventually leading to general autolysis.
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页码:2958 / 2962
页数:5
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