Dps is a nucleoid-associated protein that plays a major role in condensation of the Escherichia coli chromosome in stationary phase. Here we show that two other nucleoid-associated proteins, Fis and H-NS, can bind at the dps gene promoter and downregulate its activity. Both Fis and H-NS selectively repress the dps promoter, preventing transcription initiation by RNA polymerase containing σ 70 , the housekeeping σ factor, but not by RNA polymerase containing σ 38 , the stationary-phase σ factor. Fis represses by trapping RNA polymerase containing σ 70 at the promoter. In contrast, H-NS functions by displacing RNA polymerase containing σ 70 , but not RNA polymerase containing σ 38 . Dps levels are known to be very low in exponentially growing cells and rise sharply as cells enter stationary phase. Conversely, Fis levels are high in growing cells but fall to nearly zero in stationary-phase cells. Our data suggest a simple model to explain how the Dps-dependent super-compaction of the folded chromosome is triggered as cell growth ceases.

Selective repression by Fis and H-NS at the Escherichia coli dps promoter. Commentary

The ability of bacteria to successfully colonize a niche and to adapt to varying growth conditions relies in large parts on bacterial genome plasticity. The gain and loss of horizontally acquired genetic information as well as point mutations, intragenomic rearrangements, and large gene amplifications contribute to genomic variability. The chromosomal structure and organization can affect the efficient incorporation of foreign DNA into the chromosome and also gene expression. Genome plasticity should not only be perceived as alterations of genome content. Structural constraints affecting the accessibility and expression of genomic loci shape bacterial genomes and are thus involved in bacterial evolution.

Genome Plasticity, Bacterial

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Genome Plasticity, Bacterial