期刊
MOLECULAR CELL
卷 5, 期 1, 页码 49-57出版社
CELL PRESS
DOI: 10.1016/S1097-2765(00)80402-5
关键词
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资金
- NATIONAL CANCER INSTITUTE [P30CA021765] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R21AI039482, R01AI039482, R01AI027913] Funding Source: NIH RePORTER
- NCI NIH HHS [P30 CA 21765] Funding Source: Medline
- NIAID NIH HHS [AI27913, AI39482] Funding Source: Medline
The binding of bactericidal antibiotics like penicillins, cephalosporins, and glycopeptides to their bacterial targets stops bacterial growth but does not directly cause cell death. A second process arising from the bacteria itself is necessary to trigger endogenous suicidal enzymes that dissolve the cell wall during autolysis. The signal and the trigger pathway for this event are completely unknown. Using S. pneumoniae as a model, we demonstrate that signal transduction via the two-component system VncR/S triggers multiple death pathways. We show that the signal sensed by VncR/S is a secreted peptide, Pep(27), that initiates the cell death program. These data depict a novel model for the control of bacterial cell death.
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