Conditional Cooperativity in Toxin-Antitoxin Regulation Prevents Random Toxin Activation and Promotes Fast Translational Recovery
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Conditional Cooperativity in Toxin-Antitoxin Regulation Prevents Random Toxin Activation and Promotes Fast Translational Recovery. / Cataudella, Ilaria; Trusina, Ala; Sneppen, Kim; Gerdes, Kenn; Mitarai, Namiko.
In: Nucleic Acids Research, Vol. 40, No. 14, 11.04.2012, p. 6424-6434.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Conditional Cooperativity in Toxin-Antitoxin Regulation Prevents Random Toxin Activation and Promotes Fast Translational Recovery
AU - Cataudella, Ilaria
AU - Trusina, Ala
AU - Sneppen, Kim
AU - Gerdes, Kenn
AU - Mitarai, Namiko
PY - 2012/4/11
Y1 - 2012/4/11
N2 - 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.
AB - 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.
U2 - 10.1093/nar/gks297
DO - 10.1093/nar/gks297
M3 - Journal article
VL - 40
SP - 6424
EP - 6434
JO - Nucleic Acids Research
JF - Nucleic Acids Research
SN - 0305-1048
IS - 14
ER -
ID: 40807104