IHF is the limiting host factor in transposition of <i>Pseudomonas putida</i> transposon Tn<i>4652</i> in stationary phase

<jats:title>Summary</jats:title><jats:p>Transpositional activity of mobile elements is not constant. Conditional regulation of host factors involved in transposition may severely change the activity of mobile elements. We have demonstrated previously that transposition of Tn<jats:italic>4652</jats:italic> in <jats:italic>Pseudomonas putida</jats:italic> is a stationary phase‐specific event, which requires functional sigma S (Ilves <jats:italic>et al</jats:italic>., 2001, <jats:italic>J Bacteriol</jats:italic> 183: 5445–5448). We hypothesized that integration host factor (IHF), the concentration of which is increased in starving <jats:italic>P. putida</jats:italic>, might contribute to the transposition of Tn<jats:italic>4652</jats:italic> as well. Here, we demonstrate that transposition of Tn<jats:italic>4652</jats:italic> in stationary phase <jats:italic>P. putida</jats:italic> is essentially limited by the amount of IHF. No transposition of Tn<jats:italic>4652</jats:italic> occurs in a <jats:italic>P. putida ihfA</jats:italic>‐defective strain. Moreover, overexpression of IHF results in significant enhancement of transposition compared with the wild‐type strain. This indicates that the amount of IHF is a bottleneck in Tn<jats:italic>4652</jats:italic> transposition. Gel mobility shift and DNase I footprinting studies revealed that IHF is necessary for the binding of transposase to both transposon ends. <jats:italic>In vitro</jats:italic>, transposase can bind to inverted repeats of transposon only after the binding of IHF. The results obtained in this study indicate that, besides sigma S, IHF is another host factor that is implicated in the elevation of transposition in stationary phase.</jats:p>