In Burkholderia glumae, flagellar biosynthesis is tightly regulated by quorum sensing through the C8-HSL–TofR–QsmR signaling cascade. At low cell density, C8-HSL (N-octanoyl-homoserine lactone) is scarce, and the LuxR-type receptor protein TofR remains inactive. As the bacterial population grows, TofI synthesizes increasing amounts of C8-HSL. Once C8-HSL reaches a threshold concentration, it binds to TofR, stabilizing and activating it. The active C8-HSL–TofR complex then activates qsmR.QsmR, a LysR-type transcriptional regulator, acts as a global regulator of quorum sensing-controlled genes. Among its key targets is the flhDC operon, the master regulator of flagellar biosynthesis. Upon activation by QsmR, flhDC initiates a hierarchical transcriptional program that turns on genes encoding structural components of the flagellum, motor proteins, and associated regulatory elements necessary for motility. Thus, through this cascade, C8-HSL indirectly activates flagellar biosynthesis: it stabilizes and activates TofR, which induces QsmR, which in turn activates flhDC, culminating in the assembly of functional flagella. This quorum-sensing–dependent regulation ensures that motility is coordinated with population density, enabling B. glumae to optimize surface colonization

Quorum sensing: Octanoyl-ACP (C8-ACP) Flagellar Biosynthesis References