The putative oligosaccharide translocase SypK connects biofilm formation with quorum signaling in Vibrio fischeri.
Bottom Line: We found that overexpression of sypK, which encodes a putative oligosaccharide translocase, is sufficient to activate qrr1, and, in addition, this effect appears to depend on the kinase activity of the sensor LuxQ.Finally, we found that induction of the syp locus by overexpression of sypG was sufficient to activate qrr1 levels.Together, our results show how conditions that promote biofilm formation impact the quorum-signaling network in V. fischeri, and further highlight the integrated nature of the regulatory circuits involved in complex bacterial behaviors.
Affiliation: Department of Biochemistry and Molecular Biology, Eberly College of Science, The Pennsylvania State University, University Park, Pennsylvania, 16802; Department of Medical Microbiology and Immunology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, 53706.Show MeSH
Mentions: From these results, we have generated the model presented in Figure 9. Under conditions that result in transcription of the syp locus, the sypK gene will be expressed, leading to the formation of this putative oligosaccharide translocase within the inner membrane. While contributing to biofilm formation, SypK can also interact with the QS pathway via LuxQ. Our results in Figure 7B suggest that the levels of the K+/P− variant of LuxQ may be influenced by SypK. One interpretation of these data consistent with our other results is that SypK stabilizes the kinase form of LuxQ; however, a clear understanding of this pathway awaits a more complete study. Regardless, the net result of sypK induction is activation of the LuxU-LuxO phosphorelay and, consequently, qrr1 expression. Whether the resulting increase in LuxU phosphorylation can further enhance syp transcription via SypG (Ray and Visick 2012) remains unknown; further characterization of the signaling pathway directly controlling the syp locus is required to determine whether a potential positive feedback loop is present. Interestingly, this regulatory link between SypK and LuxQ suggests a mechanism that enables V. fischeri cells densely packed within a biofilm to activate the LuxU-LuxO phosphorelay even in the presence of AI-2, which is an autoinducer broadly used for bacterial QS.
Affiliation: Department of Biochemistry and Molecular Biology, Eberly College of Science, The Pennsylvania State University, University Park, Pennsylvania, 16802; Department of Medical Microbiology and Immunology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, 53706.