The RssAB Two-Component Signal Transduction System in Serratia marcescens Regulates Swarming Motility and Cell Envelope Architecture in Response to Exogenous Saturated Fatty Acids

Abstract

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 swarms at 30°C. Analysis of this mutant revealed that the transposon was 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 insertiondeletion mutants were constructed through homologous recombination, and the two mutants exhibited similar swarming phenotypes on LB swarming agar, in which swarming not only occurred at 37°C but also initiated at a lower cell density, on a surface with a higher agar concentration, and more rapidly than the swarming of the parent strain at 30°C. Both mutants also exhibited increased hemolysin 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 fatty acid profiles of the parent and the rssA and rssB mutants grown at 30°C or 37°C and under different nutrition conditions revealed a relationship between cellular fatty acid composition and swarming phenotypes. The cellular fatty acid profile was also observed to be affected by RssA and RssB. SFA-dependent inhibition of swarming was also observed in Proteus mirabilis, 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.

Modulation of quorum sensing in Pseudomonas aeruginosa through alteration of membrane properties

“…We have demonstrated that the shift towards increased C18 and reduced C16 fatty acids in the lptA mutant leads to reduced membrane fluidity, as measured using a fluorescent probe. The cold sensitivity and lack of motility of the lptA mutant are phenotypes consistent with a reduction in membrane fluidity (Schujman et al, 2003;Liaw et al, 2004;Lai et al, 2005).…”

“…Therefore, we can not exclude that the cold-sensitive phenotype of the lptA mutant is related to the observed decrease in PC level. Links have also been found between membrane fluidity and motility (Liaw et al, 2004;Lai et al, 2005), therefore we also looked at this phenotype in the lptA mutant. It was found that the lptA mutant was significantly impaired in both swimming (Fig.…”

Complete Genome Sequence of Uropathogenic Proteus mirabilis , a Master of both Adherence and Motility

“…Six other genes outside the flagellar locus encode methyl-accepting chemotaxis proteins (PMI1180, PMI2380, PMI2381, PMI2671, PMI2808, and PMI2809), and one aerotaxis gene, aer (PMI2813), was identified. Genes encoding several previously identified regulators of P. mirabilis flagellar motility were also located in the chromosome, including umoA (PMI3115), umoB (PMI3018), umoC (PMI1939), umoD (PMI0876) (19), rssBA (PMI1696 and PMI1697) (35), wosA (PMI0608) (25), and the rcsBCD regulatory system (PMI1729 to PMI1731) composed of genes encoding the sensor kinase RcsC, the phosphotransfer intermediate protein RcsD (YojN) (72) (also described as rsbA [42]), and the response regulator RcsB (16).…”

Heteroorganic molecules and bacterial biofilms: Controlling biodeterioration of cultural heritage

“…159 Controlled by cell-to-cell signalling molecules, N-acyl-homoserine lactones (AHLs), the production of biosurfactants such as rhamnolipids determine the pattern of the swarming colony. 160,161 In addition to their role as signalling molecules, AHLs may also have a direct function by acting as surfactants themselves, promoting surface translocation. 162 As described in the next section, evidence that the shift between migrating and sessile surface behaviour is regulated via a method of cell-to-cell communication know as quorum sensing is accruing.…”