Toxins-antitoxins: plasmid maintenance, programmed cell death, and cell cycle arrest.
Antibiotic resistance, virulence, and other plasmids in bacteria use toxin-antitoxin gene pairs to ensure their persistence during host replication. The toxin-antitoxin system eliminates plasmid-free cells that emerge as a result of segregation or replication defects and contributes to intra- and interspecies plasmid dissemination. Chromosomal homologs of toxin-antitoxin genes are widely distributed in pathogenic and other bacteria and induce reversible cell cycle arrest or programmed cell death in response to starvation or other adverse conditions. The dissection of the interaction of the toxins with intracellular targets and the elucidation of the tertiary structures of toxin-antitoxin complexes have provided exciting insights into toxin-antitoxin behavior.
Hayes
Finbarr
F
Department of Biomolecular Sciences, University of Manchester Institute of Science and Technology, Manchester M60 1QD, UK. finbarr.hayes@umist.ac.uk
D017209:Apoptosis; D001419:Bacteria / Q000235:genetics / Q000472:pathogenicity; D018407:Bacterial Physiological Phenomena; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D002453:Cell Cycle; D002876:Chromosomes, Bacterial; D004269:DNA, Bacterial / Q000378:metabolism; D010957:Plasmids
D001426:Bacterial Proteins; D004269:DNA, Bacterial