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Background  Hfq functions in post-transcriptional gene regulation in a wide range of bacteria, usually by promoting base pairing of mRNAs with  trans -encoded sRNAs. It was previously shown that Hfq down-regulates  Tn10  transposition by inhibiting  IS10  transposase expression at the post-transcriptional level. This provided the first example of Hfq playing a role in DNA transposition and led us to ask if a related transposon,  Tn5 , is similarly regulated.    Results  We show that Hfq strongly suppresses  Tn5  transposition in  Escherichia coli  by inhibiting  IS50  transposase expression. However, in contrast to the situation for  Tn10 , Hfq primarily inhibits  IS50  transposase transcription. As Hfq does not typically function directly in transcription, we searched for a transcription factor that also down-regulated  IS50  transposase transcription and is itself under Hfq control. We show that Crp (cyclic AMP receptor protein) fits these criteria as: (1) disruption of the  crp  gene led to an increase in  IS50  transposase expression and the magnitude of this increase was comparable to that observed for an  hfq  disruption; and (2) Crp expression decreased in  hfq   −  . We also demonstrate that  IS50  transposase expression and  Tn5  transposition are induced by over-expression of the sRNA SgrS and link this response to glucose limitation.    Conclusions   Tn5  transposition is negatively regulated by Hfq primarily through inhibition of  IS50  transposase transcription. Preliminary results support the possibility that this regulation is mediated through Crp. We also provide evidence that glucose limitation activates  IS50  transposase transcription and transposition.    Electronic supplementary material  The online version of this article (doi:10.1186/s13100-014-0027-z) contains supplementary material, which is available to authorized users.

Tn5 transposition in Escherichia coli is repressed by Hfq and activated by over-expression of the small non-coding RNA SgrS