Abstract

The natural physiological regime of the soil bacterium Pseudomonas putida involves incessant exposure to endogenous metabolic conflicts and environmental physicochemical insults. Yet, the role of assisted small RNA-mRNA pairing in the stress tolerance super-phenotype that is the trademark of this bacterium has not been accredited. We have thoroughly explored the physiological consequences -in particular those related to exogenous stress - of deleting the hfq gene of P. putida, which encodes the major RNA chaperone that promotes sRNA-target mRNA interactions. While the overall trend was a general weakening of every robustness descriptor of the Δhfq strain, growth parameters and production of central metabolic enzymes were comparatively less affected than other qualities that depend directly on energy status (e.g. motility, DNA repair). The overall catalytic vigour of the mutant decreased to < 20% than the wild-type strain, as estimated from the specific growth rate of cells carrying the catabolic TOL plasmid pWW0 for m-xylene biodegradation. Several loss-of-function phenotypes could be traced to the effect of the Δhfq deletion on the intracellular contents of the stationary sigma factor RpoS. It thus seems that Hfq, while not indispensable for any essential function, contributes to shape the environmental lifestyle of P. putida.

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