Document Detail

Conditional cooperativity in toxin-antitoxin regulation prevents random toxin activation and promotes fast translational recovery.
MedLine Citation:
PMID:  22495927     Owner:  NLM     Status:  MEDLINE    
Many toxin-antitoxin (TA) loci are known to strongly repress their own transcription. This auto-inhibition is often called 'conditional cooperativity' as it relies on cooperative binding of TA complexes to operator DNA that occurs only when toxins are in a proper stoichiometric relationship with antitoxins. There has recently been an explosion of interest in TA systems due to their role in bacterial persistence, however the role of conditional cooperativity is still unclear. We reveal the biological function of conditional cooperativity by constructing a mathematical model of the well studied TA system, relBE of Escherichia coli. We show that the model with the in vivo and in vitro established parameters reproduces experimentally observed response to nutritional stress. We further demonstrate that conditional cooperativity stabilizes the level of antitoxin in rapidly growing cells such that random induction of relBE is minimized. At the same time it enables quick removal of free toxin when the starvation is terminated.
Ilaria Cataudella; Ala Trusina; Kim Sneppen; Kenn Gerdes; Namiko Mitarai
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-04-11
Journal Detail:
Title:  Nucleic acids research     Volume:  40     ISSN:  1362-4962     ISO Abbreviation:  Nucleic Acids Res.     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-08-08     Completed Date:  2012-11-05     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  0411011     Medline TA:  Nucleic Acids Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  6424-34     Citation Subset:  IM    
Center for Models of Life, Niels Bohr Institute, University of Copenhagen, Blegdamsvej 17, DK-2100 Copenhagen, Denmark.
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MeSH Terms
Amino Acids / metabolism
Bacterial Toxins / genetics*,  metabolism
Escherichia coli / genetics,  metabolism
Escherichia coli Proteins / genetics*,  metabolism
Gene Expression Regulation, Bacterial*
Models, Genetic*
Protein Biosynthesis
Transcription, Genetic
Reg. No./Substance:
0/Amino Acids; 0/Bacterial Toxins; 0/Escherichia coli Proteins; 0/RelB protein, E coli; 0/RelE protein, E coli

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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