Your browser doesn't support javascript.
loading
Demonstration of the role of cell wall homeostasis in Staphylococcus aureus growth and the action of bactericidal antibiotics.
Salamaga, Bartlomiej; Kong, Lingyuan; Pasquina-Lemonche, Laia; Lafage, Lucia; von Und Zur Muhlen, Milena; Gibson, Josie F; Grybchuk, Danyil; Tooke, Amy K; Panchal, Viralkumar; Culp, Elizabeth J; Tatham, Elizabeth; O'Kane, Mary E; Catley, Thomas E; Renshaw, Stephen A; Wright, Gerard D; Plevka, Pavel; Bullough, Per A; Han, Aidong; Hobbs, Jamie K; Foster, Simon J.
Afiliación
  • Salamaga B; School of Biosciences, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Kong L; The Florey Institute for Host-Pathogen Interactions, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Pasquina-Lemonche L; State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen 361102, China.
  • Lafage L; The Florey Institute for Host-Pathogen Interactions, University of Sheffield, Sheffield S102TN, United Kingdom.
  • von Und Zur Muhlen M; Department of Physics and Astronomy, University of Sheffield, Sheffield S37RH, United Kingdom.
  • Gibson JF; School of Biosciences, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Grybchuk D; The Florey Institute for Host-Pathogen Interactions, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Tooke AK; School of Biosciences, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Panchal V; The Florey Institute for Host-Pathogen Interactions, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Culp EJ; School of Biosciences, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Tatham E; The Florey Institute for Host-Pathogen Interactions, University of Sheffield, Sheffield S102TN, United Kingdom.
  • O'Kane ME; The Bateson Centre, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Catley TE; Central European Institute of Technology, Masaryk University, Brno 60177, Czech Republic.
  • Renshaw SA; School of Biosciences, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Wright GD; The Florey Institute for Host-Pathogen Interactions, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Plevka P; School of Biosciences, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Bullough PA; The Florey Institute for Host-Pathogen Interactions, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Han A; M. G. DeGroote Institute for Infectious Disease Research, David Braley Centre for Antibiotic Discovery, Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON L8S4L8, Canada.
  • Hobbs JK; School of Biosciences, University of Sheffield, Sheffield S102TN, United Kingdom.
  • Foster SJ; The Florey Institute for Host-Pathogen Interactions, University of Sheffield, Sheffield S102TN, United Kingdom.
Proc Natl Acad Sci U S A ; 118(44)2021 11 02.
Article en En | MEDLINE | ID: mdl-34716264
Bacterial cell wall peptidoglycan is essential, maintaining both cellular integrity and morphology, in the face of internal turgor pressure. Peptidoglycan synthesis is important, as it is targeted by cell wall antibiotics, including methicillin and vancomycin. Here, we have used the major human pathogen Staphylococcus aureus to elucidate both the cell wall dynamic processes essential for growth (life) and the bactericidal effects of cell wall antibiotics (death) based on the principle of coordinated peptidoglycan synthesis and hydrolysis. The death of S. aureus due to depletion of the essential, two-component and positive regulatory system for peptidoglycan hydrolase activity (WalKR) is prevented by addition of otherwise bactericidal cell wall antibiotics, resulting in stasis. In contrast, cell wall antibiotics kill via the activity of peptidoglycan hydrolases in the absence of concomitant synthesis. Both methicillin and vancomycin treatment lead to the appearance of perforating holes throughout the cell wall due to peptidoglycan hydrolases. Methicillin alone also results in plasmolysis and misshapen septa with the involvement of the major peptidoglycan hydrolase Atl, a process that is inhibited by vancomycin. The bactericidal effect of vancomycin involves the peptidoglycan hydrolase SagB. In the presence of cell wall antibiotics, the inhibition of peptidoglycan hydrolase activity using the inhibitor complestatin results in reduced killing, while, conversely, the deregulation of hydrolase activity via loss of wall teichoic acids increases the death rate. For S. aureus, the independent regulation of cell wall synthesis and hydrolysis can lead to cell growth, death, or stasis, with implications for the development of new control regimes for this important pathogen.
Asunto(s)
Palabras clave

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Staphylococcus aureus / Peptidoglicano / Pared Celular Idioma: En Revista: Proc Natl Acad Sci U S A Año: 2021 Tipo del documento: Article País de afiliación: Reino Unido Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Staphylococcus aureus / Peptidoglicano / Pared Celular Idioma: En Revista: Proc Natl Acad Sci U S A Año: 2021 Tipo del documento: Article País de afiliación: Reino Unido Pais de publicación: Estados Unidos