In this system, we employ two fundamental circuits: the LuxI/LuxR system and the LasI/LasR system. Our design designates the peptide producer as the predator and the controller as the prey. <br>
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When the prey density is low, predator cells undergo apoptosis due to the constitutive expression of the suicide
gene (<i>ccdB</i>). In the prey cells, LuxI synthesizes an acyl-homoserine lactone (AHL) known as 3OC6HSL.
As prey density increases, 3OC6HSL accumulates in the extracellular environment and, at sufficiently high
gene (<i>ccdB</i>). In the prey cells, LuxI synthesizes an acyl-homoserine lactone (AHL) known as 3OC<sub>6</sub>HSL.
As prey density increases, 3OC<sub>6</sub>HSL accumulates in the extracellular environment and, at sufficiently high
concentrations, binds to the LuxR transcriptional regulator in predator cells. This binding leads to the increased
expression of the antidote gene (<i>ccdA</i>), rescuing the predator cells from apoptosis. Conversely, LasI in the predator cells produces another AHL, 3OC12HSL, which diffuses into the prey cells and binds with LasR, activating the expression of the ccdB gene to initiate "hunting".
expression of the antidote gene (<i>ccdA</i>), rescuing the predator cells from apoptosis. Conversely, LasI in the predator cells produces another AHL, 3OC<sub>12</sub>HSL, which diffuses into the prey cells and binds with LasR, activating the expression of the ccdB gene to initiate "hunting".
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Therefore, when the controller density is low, the peptide producers will die. Only when the controller reaches a certain density can the peptide producers survive. If the density of the peptide producers becomes too high, the controllers are "hunted," reducing their density and causing the death of the peptide producers once again. This dynamic system ensures that our bacteria maintain a specific range of densities.
