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Induction of autolysis in Streptococcus faecium
M E Carvalho1, M H Gonçalves, M T Silva
1Instituto de Ciências Biomédicas, Abel Salazar, Largo da Escola Médica, Porto, Portugal.
Journal of General Microbiology
|April 1, 1987
Summary
Autolysis in Streptococcus faecium can be induced by freezing-thawing in Tris buffer, activating endogenous bacterial autolysins. This process causes cell damage and leakage, but is inhibited by specific agents.
Area of Science:
- Microbiology
- Bacterial Autolysis
Background:
- Autolysis is a critical process in bacterial cell death and remodeling.
- Understanding the triggers and mechanisms of bacterial autolysis is essential for controlling microbial populations.
Purpose of the Study:
- To investigate the induction of autolysis in Streptococcus faecium using physical and chemical methods.
- To identify the role of endogenous bacterial autolysins in this process.
Main Methods:
- Exponential-phase Streptococcus faecium cells were pretreated by freezing-thawing in Tris buffer.
- Incubation at 37 degrees C in Tris buffer was performed to induce autolysis.
- Autolysis was assessed in the presence of autolysin inhibitors and in autolytic-defective mutants.
- Cell damage and leakage of intracellular components (K+, UV-absorbing substances) were measured.
Main Results:
- Freezing-thawing in Tris buffer effectively promoted autolysis in S. faecium, dependent on Tris concentration.
- Pretreatment caused ultrastructural damage, K+ loss, and leakage of UV-absorbing components.
- Autolysis was inhibited by N-bromosuccinimide and by prior growth in chloramphenicol or tetracycline.
- Autolytic-defective mutants did not lyse, confirming the role of endogenous autolysin.
- Imidazole could also induce autolysis, though to a lesser extent than Tris.
Conclusions:
- The lysis of S. faecium induced by freezing-thawing in Tris buffer is mediated by endogenous bacterial autolysin activity.
- Tris buffer acts as an inducer and potentially an activator for bacterial autolysis.
- This study provides insights into the regulation and induction of bacterial autolysis.