賴信志2006-07-262018-07-062006-07-262018-07-062000http://ntur.lib.ntu.edu.tw//handle/246246/27754We have identified and characterized a pair of luxI/R homologues termed smaI/R from Serratia marcescens SS-1. From cell-free culture supernatants, two N-acyl homoserine lactone (AHL) molecules, N-(3-oxohexanoyl) homoserine lactone (C6- HSL) and N-(3-oxooctanoyl) homoserine lactone (C8-HSL), were chemically characterized. Unlike the swrI/R system of S. liquefaciens, the presence of multicopy, plasmid-encoded smaR inhibits the spreading of S. marcescens SS-1. Further study showed that production of biosurfactants and expression of one of the virulence factors, nuclease gene nucA, were also repressed. These repressed phenotypes were specifically de-repressed by AHL signals produced by smaI. Different modifications of the AHL signals had either without or inhibitory effect on S. marcescens SS-1 spreading. Long chain AHLs show a trend of competition with the native AHL signals synthesized by SmaI. Mutation of S. marcescens chromosomal smaR shortens the time before spreading motility is initiated for 1 hour. On the contrary, mutation of smaI significantly delays initiation of spreading. Plasmid-encoded PsmaI::luxAB and PsmaR::luxAB reporter of smaI and smaR transcription, respectively, are constructed. Using this reporter system, the expression patterns of smaI and smaR following the growth in liquid broth culture were monitored. Further studies showed the evidence of smaR positive autoregulation, and that AHL signals were constitutively produced in the log phase and its production was turned off as the cells entered into stationary phase. Our findings indicate that smaI/R quorum-sensing system is a component of the complex regulatory network that controls multicellular behaviour of of S. marcescens.application/pdf86324 bytesapplication/pdfzh-TW國立臺灣大學醫學院醫學檢驗暨生物技術學系journal articlehttp://ntur.lib.ntu.edu.tw/bitstream/246246/27754/1/892320B002088.pdf