Chemotaxis towards carbohydrates is mediated, in enteric bacteria, either by the transport-independent, methylation-dependent chemotaxis pathway or by transport and phosphorylation via the phosphoenolpyruvate (PEP)-dependent phosphotransferase system (PTS). This study shows that Rhodobacter sphaeroides is chemotactic to a range of carbohydrates but the response involves neither the classical methyl-accepting chemotaxis protein (MCP) pathway nor the PTS transport pathway. The chemoattractant fructose was transported by a fructose-specific PTS system, but transport through this system did not appear to cause a chemotactic signal. Chemotaxis to sugars was inducible and occurred with the induction of carbohydrate transport systems and with substrate incorporation. A mutation of the glucose-6-phosphate dehydrogenase gene (zyyf) inhibited chemotaxis towards substrates metabolized by this pathway although transport was unaffected. Chemotaxis to other, unrelated, chemoattractants (e.g. succinate) was unaffected. These data, in conjunction with the fact that mannitol and fructose (which utilize different transport pathways) compete in chemotaxis assays, suggest that in R. sphaeroides the chemotactic signal is likely to be generated by metabolic intermediates or the activities of the electron-transport chain and not by a cellsurface receptor or the rate or mode of substrate transport.

Various factors involved in haemostasis also regulate the development of new blood vessels by a process called angiogenesis. Enzymatic cleavage of fibrin yields a variety of fibrin degradation products, particularly in areas of intense angiogenesis such as in healing wounds and active atherosclerotic plaques. One of these, fibrin fragment E (FnE), is a potent angiogenic factor in the chick chorioallantoic membrane assay of angiogenesis. Here, we extend these studies to show that FnE stimulates the proliferation, migration and differentiation of human dermal microvascular endothelial cells (HuDMECs) in vitro, both in the absence and presence of such additional endothelial growth factors as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). We also show that these stimulatory effects occur at concentrations of the protein known to be present in angiogenic tissues in vivo. FnE enhanced the angiogenic effects of VEGF or bFGF, indicating a possible synergy between the signalling pathways used by these three angiogenic factors.