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Gene Review

atl  -  autolysin

Staphylococcus aureus RF122

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Disease relevance of atl


High impact information on atl

  • Thus, changes in cell-wall cross-linking and/or autolytic activity can modulate PLA2 action either by affecting enzyme access to membrane PL or by the coupling of massive PL degradation to autolysin-dependent killing and bacterial lysis or both [6].
  • The surfactant fraction readily killed pneumococci containing ethanolamine or the autolysin-defective transformant, and studies with tritiated methyl-D-glucose loading and release showed that killing was associated with increased bacterial cell membrane permeability [7].
  • Lysis of pneumococci by the surfactant fraction appeared to be mediated by a detergent-like activation of pneumococcal autolysin, in that bacteriolysis was prevented by substitution of ethanolamine for choline in pneumococcal cell walls, and a pneumococcal transformant that lacked autolysin was not lysed [7].
  • Thus, it appears that the repeat domains direct pro-Atl, amidase and glucosaminidase to a specific receptor at the equatorial surface ring of staphylococci, thereby allowing localized peptidoglycan hydrolysis and separation of the dividing cells [4].
  • The open reading frame for atl was 3768 bp in length, encoding a deduced protein of 1256 amino acids and molecular size of 137,381 Da [1].

Chemical compound and disease context of atl


Biological context of atl

  • The formation of a ring structure of atl gene products may be required for efficient partitioning of daughter cells after cell division [11].
  • Disruption of the major autolysin gene, atl, did not produce any effect on the biofilm phenotype of an arlRS mutant [12].
  • The transcription initiation site was located at an adenine residue 33-nt upstream from the putative atl start codon [13].
  • Growth of the methicillin-susceptible strain H in the presence of subinhibitory concentrations of cefoxitin, a specific inhibitor of penicillin-binding protein (PBP) 4, caused a substantial decrease in PG cross-linking and O acetylation and increased susceptibilities of PCW and PG to LiCl-extracted autolysin and to lysozyme [14].
  • When added to S. aureus cultures at different stages of bacterial growth, quinupristin/dalfopristin reduced in a dose-dependent manner the release of specific virulence factors (e.g. autolysin, protein A, alpha- and beta-haemolysins, lipases) [15].

Anatomical context of atl

  • The distribution of the gold particles on the surface of protoplast cells and the association of the gold particles with fibrous materials extending from the cells suggested that some atl gene products were associated with a cellular component extending from the cell membrane, such as lipoteichoic acid [11].
  • In contrast, the detergent had no effect on the activity of autolysins in cell-free systems, and growth in the presence of Triton X-100 did not alter either the cellular autolysin activity or the susceptibility of cell walls to exogenous lytic enzymes [16].

Associations of atl with chemical compounds

  • A number of observations including mass spectrometric analysis suggest that the satellites are the products of an N-acetylglucosaminidase activity that differs from the atl gene product and that appears to be involved with modification of the glycan strand structure [17].
  • Growth of the methicillin-susceptible strain DU4916S in the presence of methicillin yielded PCW and PG that showed small increases in susceptibilities to LiCl-extracted autolysin and to lysozyme and a small decrease in PG cross-linking [14].
  • Triton X-100 stimulated autolysin activity of S. aureus cells under nongrowing conditions, and this lytic response was markedly reduced in energy-poisoned cells [16].
  • Finally, the arlS mutant showed a dramatic decrease of extracellular proteolytic activity, including serine protease activity, in comparison to the wild-type strain and the complemented mutant, and cells grown in the presence of phenylmethylsulfonyl fluoride (a serine protease inhibitor) showed an increased autolysin activity [18].
  • The release of lipoteichoic acid (LTA), a modulator of autolysin activity, from penicillin-treated bacteria was inhibited by heparin and dextran sulphate [19].

Regulatory relationships of atl

  • Besides V8 protease (StsP) and Hlb already described to be regulated by the sar locus new putatively sarA-dependent proteins were identified, e.g. glycerolester hydrolase and autolysin both down-regulated in the sarA mutant, and aureolysin, staphylokinase, staphopain and format tetrahydrofolate lyase up-regulated in the mutant [20].

Other interactions of atl


Analytical, diagnostic and therapeutic context of atl

  • The cell surface localization of the atl gene products was investigated by immunoelectron microscopy using anti-62-kDa N-acetylmuramyl-L-alanine amidase or anti-51-kDa endo-beta-N-acetylglucosaminidase immunoglobulin G [11].
  • Lysostaphin MICs were determined by a broth microdilution technique and reverse transcriptase PCR was used to compare atl expression levels in all isolates [22].
  • Immunoblotting studies suggest that these are all atl gene products: the 138-kDa protein is an ATL with a cleaved signal sequence; the 115- and 85-kDa proteins are intermediates; and the 51- and 62-kDa proteins are cell-associated 51-kDa GL and 62-kDa AM, respectively [23].
  • The objective of our study was to examine the effect of oxacillin, chloramphenicol and tetracycline on autolysis, peptidoglycan hydrolase profiles and transcription of atl encoding the major S. aureus autolysin on cells grown in the presence of minimum inhibitory concentrations of the antibiotics [10].
  • A Staphylococcus aureus autolysin that has an N-acetylmuramoyl-L-alanine amidase domain and an endo-beta-N-acetylglucosaminidase domain: cloning, sequence analysis, and characterization [1].


  1. A Staphylococcus aureus autolysin that has an N-acetylmuramoyl-L-alanine amidase domain and an endo-beta-N-acetylglucosaminidase domain: cloning, sequence analysis, and characterization. Oshida, T., Sugai, M., Komatsuzawa, H., Hong, Y.M., Suginaka, H., Tomasz, A. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  2. Identification and molecular characterization of an N-acetylmuramyl-L-alanine amidase Sle1 involved in cell separation of Staphylococcus aureus. Kajimura, J., Fujiwara, T., Yamada, S., Suzawa, Y., Nishida, T., Oyamada, Y., Hayashi, I., Yamagishi, J., Komatsuzawa, H., Sugai, M. Mol. Microbiol. (2005) [Pubmed]
  3. Molecular characterization of an atl null mutant of Staphylococcus aureus. Takahashi, J., Komatsuzawa, H., Yamada, S., Nishida, T., Labischinski, H., Fujiwara, T., Ohara, M., Yamagishi, J., Sugai, M. Microbiol. Immunol. (2002) [Pubmed]
  4. Targeting of muralytic enzymes to the cell division site of Gram-positive bacteria: repeat domains direct autolysin to the equatorial surface ring of Staphylococcus aureus. Baba, T., Schneewind, O. EMBO J. (1998) [Pubmed]
  5. Evidence for autolysin-mediated primary attachment of Staphylococcus epidermidis to a polystyrene surface. Heilmann, C., Hussain, M., Peters, G., Götz, F. Mol. Microbiol. (1997) [Pubmed]
  6. Cell-wall determinants of the bactericidal action of group IIA phospholipase A2 against Gram-positive bacteria. Foreman-Wykert, A.K., Weinrauch, Y., Elsbach, P., Weiss, J. J. Clin. Invest. (1999) [Pubmed]
  7. Detection and partial characterization of antibacterial factor(s) in alveolar lining material of rats. Coonrod, J.D., Yoneda, K. J. Clin. Invest. (1983) [Pubmed]
  8. Transcriptomic and functional analysis of an autolysis-deficient, teicoplanin-resistant derivative of methicillin-resistant Staphylococcus aureus. Renzoni, A., Barras, C., François, P., Charbonnier, Y., Huggler, E., Garzoni, C., Kelley, W.L., Majcherczyk, P., Schrenzel, J., Lew, D.P., Vaudaux, P. Antimicrob. Agents Chemother. (2006) [Pubmed]
  9. Localized perforation of the cell wall by a major autolysin: atl gene products and the onset of penicillin-induced lysis of Staphylococcus aureus. Sugai, M., Yamada, S., Nakashima, S., Komatsuzawa, H., Matsumoto, A., Oshida, T., Suginaka, H. J. Bacteriol. (1997) [Pubmed]
  10. Effects of oxacillin and tetracycline on autolysis, autolysin processing and atl transcription in Staphylococcus aureus. Ledala, N., Wilkinson, B.J., Jayaswal, R.K. Int. J. Antimicrob. Agents (2006) [Pubmed]
  11. An autolysin ring associated with cell separation of Staphylococcus aureus. Yamada, S., Sugai, M., Komatsuzawa, H., Nakashima, S., Oshida, T., Matsumoto, A., Suginaka, H. J. Bacteriol. (1996) [Pubmed]
  12. Staphylococcus aureus develops an alternative, ica-independent biofilm in the absence of the arlRS two-component system. Toledo-Arana, A., Merino, N., Vergara-Irigaray, M., Débarbouillé, M., Penadés, J.R., Lasa, I. J. Bacteriol. (2005) [Pubmed]
  13. Expression analysis of the autolysin gene (atl) of Staphylococcus aureus. Oshida, T., Takano, M., Sugai, M., Suginaka, H., Matsushita, T. Microbiol. Immunol. (1998) [Pubmed]
  14. Effects of growth of methicillin-resistant and -susceptible Staphylococcus aureus in the presence of beta-lactams on peptidoglycan structure and susceptibility to lytic enzymes. Qoronfleh, M.W., Wilkinson, B.J. Antimicrob. Agents Chemother. (1986) [Pubmed]
  15. Subinhibitory quinupristin/dalfopristin attenuates virulence of Staphylococcus aureus. Koszczol, C., Bernardo, K., Krönke, M., Krut, O. J. Antimicrob. Chemother. (2006) [Pubmed]
  16. Use of resistant mutants to study the interaction of triton X-100 with Staphylococcus aureus. Raychaudhuri, D., Chatterjee, A.N. J. Bacteriol. (1985) [Pubmed]
  17. Characterization of Staphylococcus aureus cell wall glycan strands, evidence for a new beta-N-acetylglucosaminidase activity. Boneca, I.G., Huang, Z.H., Gage, D.A., Tomasz, A. J. Biol. Chem. (2000) [Pubmed]
  18. A new two-component regulatory system involved in adhesion, autolysis, and extracellular proteolytic activity of Staphylococcus aureus. Fournier, B., Hooper, D.C. J. Bacteriol. (2000) [Pubmed]
  19. Effects of mucopolysaccharides on penicillin-induced lysis of Staphylococcus aureus. Kiriyama, T., Miyake, Y., Sugai, M., Kobayashi, K., Yoshiga, K., Takada, K., Suginaka, H. J. Med. Microbiol. (1987) [Pubmed]
  20. Extracellular proteins of Staphylococcus aureus and the role of SarA and sigma B. Ziebandt, A.K., Weber, H., Rudolph, J., Schmid, R., Höper, D., Engelmann, S., Hecker, M. Proteomics (2001) [Pubmed]
  21. Latent LytM at 1.3A resolution. Odintsov, S.G., Sabala, I., Marcyjaniak, M., Bochtler, M. J. Mol. Biol. (2004) [Pubmed]
  22. Reduced expression of the atl autolysin gene and susceptibility to autolysis in clinical heterogeneous glycopeptide-intermediate Staphylococcus aureus (hGISA) and GISA strains. Wootton, M., Bennett, P.M., MacGowan, A.P., Walsh, T.R. J. Antimicrob. Chemother. (2005) [Pubmed]
  23. Subcellular localization of the major autolysin, ATL and its processed proteins in Staphylococcus aureus. Komatsuzawa, H., Sugai, M., Nakashima, S., Yamada, S., Matsumoto, A., Oshida, T., Suginaka, H. Microbiol. Immunol. (1997) [Pubmed]
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