FIGURE 4.

Quorum sensing regulatory system in D. shibae. (A) 3-oxo C14 HSL might be detected by the histidine kinase CckA or another sensor protein (red arrow) resulting in a phosphorylation cascade activating CtrA (blue) and subsequently its target genes (continuous arrows). LuxI₂ might restrict GTA expression to a subpopulation (inhibiting arrow). The SOS stress response regulator LexA and CtrA (dashed arrows) regulate overlapping traits. The activation of LexA by RecA binding to ssDNA induces autoproteolysis of the stress regulator (green). (B) Possible impact of QS induced replication within the first 2 h post-induction on ori and ter located genes. Copy-number differences might alter the transcriptional balance of QS regulators close to origin and terminus of replication (left panel). Hemi-methylation during replication might impact transcription of CtrA-target genes (right panel). (C) Proposed model for the early response of D. shibae toward QS signaling: AHL detection results in fast activation of CtrA followed by an induction of replication as well as QS and c-di-GMP synthesizing genes. The increase in CtrA and its phosphorylation by CckA leads to repression of replication and initiates cell division and differentiation. The autoinducer synthase LuxI₂ is the key factor in the decision making between GTA producing self-sacrificing cells and cells which form flagella, pili, and become competent for uptake of GTA-DNA between 2 and 4 h after induction. Following the stop of replication for 6 h, increasing c-di-GMP levels induce CckA mediated dephosphorylation of CtrA in some cells that start replicating again. The late induction of the SOS response could stimulate recombination of transferred DNA.