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Growth control switch by a DNA damage-inducible toxin-antitoxin system in Caulobacter

ABSTRACT: Bacterial toxin-antitoxin systems (TASs) are thought to respond to various stresses, often inducing growth-arrested (persistent) sub-populations of cells whose housekeeping functions are inhibited. However, it is not always clear whether specific targets of orthologous RNAse toxins are responsible for their phenotypic effect, which has made it difficult to accurately place the multitude of TASs within cellular and adaptive regulatory networks. Here we show that the TAS HigBA can promote and inhibit bacterial growth dependent on the dosage of HigB, a toxin regulated by the DNA damage (SOS) repressor LexA in addition to its antitoxin HigA, and the target selectivity of HigB’s mRNA cleavage activity. HigB reduced the expression of an efflux pump that is toxic to a polarity control mutant, cripples the growth of cells lacking LexA and targets the cell cycle circuitry. Thus, TASs can have outcome switching activity in bacterial adaptive (stress) and systemic (cell cycle) networks.

ORGANISM(S): Caulobacter vibrioides NA1000

PROVIDER: GSE76721 | GEO | 2016/02/17

SECONDARY ACCESSION(S): PRJNA308454

REPOSITORIES: GEO

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Growth control switch by a DNA damage-inducible toxin-antitoxin system in Caulobacter

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