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Team:XMU-China/Data
From 2011.igem.org
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=='''How our devices work'''== | =='''How our devices work'''== | ||
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Figure 1: The synthesis of LuxR protein and the signalling molecule N-acyl-homoserine lactone (AHL) is induced by adding Isopropyl β-D-1-thiogalactopyranoside (IPTG). The AHL accumulates in the experimental medium and inside the cells as the cell density increases. At sufficiently high concentrations, it binds and activates the LuxR transcriptional regulator, which in turn induces the expression of a killer gene ''ccdB'' under the control of a promoter lux pR. Sufficiently high levels of the killer protein cause cell death. This circuit programmes a bacterial population to maintain a cell density that is lower than the limits imposed by the environment. | Figure 1: The synthesis of LuxR protein and the signalling molecule N-acyl-homoserine lactone (AHL) is induced by adding Isopropyl β-D-1-thiogalactopyranoside (IPTG). The AHL accumulates in the experimental medium and inside the cells as the cell density increases. At sufficiently high concentrations, it binds and activates the LuxR transcriptional regulator, which in turn induces the expression of a killer gene ''ccdB'' under the control of a promoter lux pR. Sufficiently high levels of the killer protein cause cell death. This circuit programmes a bacterial population to maintain a cell density that is lower than the limits imposed by the environment. | ||
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Figure 2: | Figure 2: | ||
Revision as of 22:42, 5 October 2011
