一個新的調控Serratia marcescens表面移行及毒素因子訊號傳遞系統之研究

Serratia marcescens swarms at 30°C, but not at 37°C on a nutrient rich (LB) agar surface. Mini-Tn5 mutagenesis of S. marcescens CH-1 yielded a mutant (WC100) that swarms not only vigorously at 37°C, but also earlier and faster than the parent strain at 30°C. Analysis of this mutant revealed that the transposon had inserted into a gene (rssA) predicted to encode a bacterial two component signal transduction sensor kinase, upstream of which, a potential response regulator gene (rssB) was located. rssA and rssB insertion-deletion mutants were constructed through homologous recombination and both exhibited similar swarming phenotypes on LB swarming agar whereby swarming not only occurs at 37°C, but also initiates at a lower cell density, on a surface of higher agar concentration and more rapidly than the parent strain at 30°C. Both mutants also exhibited increased haemolysin activity and altered cell surface topologies compared with the parent CH-1 strain. Temperature and certain saturated fatty acids (SFAs) were found to negatively regulate S. marcescens swarming via the action of RssA-RssB. Analysis of the respective fatty acid profiles of the parent, rssA and rssB mutants grown at 30oC or 37oC and different nutrition conditions revealed a relationship between cellular fatty acid composition and swarming phenotypes. The cellular fatty acid profile is further observed to be affected by RssA and RssB. SFA-dependent inhibition of swarming was also observed in Proteus mirabilis and Salmonella typhimurium, suggesting that either SFAs per se or the modulation of cellular fatty acid composition and hence homeostasis of membrane fluidity may be a conserved mechanism for regulating swarming motility in Gram negative bacteria