Bridged filaments of histone-like nucleoid structuring protein pause RNA polymerase and aid termination in bacteria

摘要

Genes—which are made of DNA—contain the genetic blueprint of an organism. Different genes are switched on (expressed) at various points in an organism's life when they are needed. When a gene is switched on or ‘expressed’, the DNA is copied using molecules of ribonucleic acid (RNA) that can then be used as templates to make proteins. One way that the expression of genes can be controlled is by the way that DNA is packaged in cells. In humans and other eukaryotic organisms, DNA is packaged within groups or ‘complexes’ of proteins called histones. The histones can interact with the cellular machinery that moves along the gene and makes the RNA copies. In doing so, the histones can alter the length of the RNA copies, and if the RNAs are too short, they will not be used to make proteins so the gene is effectively switched off. We know much less about how DNA packaging in bacteria cells affects gene expression. There are many different DNA packaging complexes in bacteria and they are less stable than the histones in eukaryotes, which makes them harder to study. In the bacteria Escherichia coli, the main DNA packaging protein is the histone-like structuring protein (H-NS). This protein binds to the DNA at select sites and forms filaments that can link to each other to form bridges between different stretches of DNA. In this study, Kotlajich et al. found that the bridged filaments formed by the H-NS protein interfere with the production of RNA copies. It is normal for the enzyme that makes RNA copies from DNA—called RNA polymerase—to make short pauses while it moves along the DNA. However, the bridged filaments made by H-NS cause RNA polymerase to pause for longer periods of time. These delays provide more time for another protein that halts gene copying to bind to the site where the RNA polymerase has paused, leading to RNA molecules that are too short to make proteins. It has previously been shown that there is less bridging between H-NS filaments in some bacteria when they are grown in warmer temperatures—around 37°C—than when they are grown in cooler temperatures of around 20–30°C. This may allow bacteria that cause diseases in animals to increase the expression of genes that help them outwit the host's defenses and to resist antibiotic treatments when they enter a warm animal body from a colder environment.