Widespread distribution of deletions of the bgl operon in natural isolates of Escherichia coli

A deletion that includes the bgl (beta-glucoside utilization) operon of Escherichia coli was originally detected in several rarely occurring natural isolates that utilize cellobiose. Here I show that bgl deletions are present in 95% of the Cel+ isolates obtained from diverse sources. They are also present in 29% of the Cel- strains in two different collections of natural isolates of E. coli. At least three versions of bgl deletions are present in E. coli populations. In the most common version approximately 8 kb of DNA around the bgl region of E. coli K12 is replaced by a specific 6.5-kb DNA fragment. In another version a deletion of similar length is not replaced by the same sequence. A third version involves deletion of approximately 14 kb without the replacement fragment being present. The distribution of these deletions suggests that the version 1 deletion occurred very early in the history of E coli. It also appears likely that there is selection for bgl deletions in Cel+ strains of E. coli. The presence of the version 1 deletion within distantly related phylogenetic groups of E. coli provides evidence for recombination within natural populations of E coli.      

Selective suppression of growth factor-induced cell cycle gene expression by Na+/H+ antiport inhibitors.

Activation of Na+/H+ exchange activity is a ubiquitous response to growth factors and has been implicated in the mitogenic response. Little is known of how the antiport influences events in the nucleus which ultimately control the cell cycle. Using potent Na+/H+ exchange inhibitors we show for normal mouse bone marrow-derived macrophages that this activity is required for the colony-stimulating factor-1-induced gene expression of the M1 and M2 subunits of ribonucleotide reductase, an enzyme critical for DNA synthesis. Suppression of M1 and M2 mRNA levels occurred when the inhibitors were added up to 8 h after the growth factor, mirroring their ability to prevent entry into S phase at similar times. Antiport activity was not required for the induction of other genes associated with cell cycle progression including proliferating cell nuclear antigen and the G1 cyclin, CYL1. These results highlight the differential expression of various cell cycle-associated genes and demonstrates that non-coordinate regulation of CYL1 cyclin and DNA synthesis gene expression can occur. The selective dependence of ribonucleotide reductase subunit gene expression on Na+/H+ exchange activity may provide a biochemical basis for the requirement of persistent antiporter activity during G1 for subsequent entry into S phase.