Abstract

The supercoiling of DNA in the bacterial cell is controlled, to a first approximation, by the opposing activities of two enzymes, DNA gyrase and DNA topoisomerase 1. Recent studies have shown that the level of plasmid and chromosomal DNA supercoiling is not constant but varies in response to a variety of environmental signals such as temperature, osmolarity and oxygen availability (Higgins et al., 1988; Dorman et al., 1988). Furthermore, these changes in DNA topology are responsible for the specific induction or repression of gene expression in response to these environmental signals. There is a class of 'stress-regulated' genes whose expression is influenced by a wide variety of environmental signals for which changes in DNA supercoiling play a central role in the regulation. Superimposed on this global control mechanism are the more specific regulatory processes with which we are all familiar. This supercoiling regulation of gene expression plays a central role in the control of bacterial virulence (Dorman et al., 1990.) Very recent data (Hulton et al., 1990) have shown that the osmZ gene, which plays a key role in supercoiling regulation in response to environmental stresses, encodes 'histone-like protein H1 '. This is an abundant, non-specific DNA binding protein which is tightly associated with the bacterial nucleoid. Preliminary data suggest that altered binding of this protein to DNA in response to environmental stresses plays a role in the regulation of DNA supercoiling and gene expression. It is becoming ever more apparent that an understanding of bacterial chromatin structure is crucial for understanding the underlying mechanisms by which gene expression is controlled. Our current understanding of chromosome structure and organization will be discussed. References

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