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. 2009 Nov 30;187(5):589–596. doi: 10.1083/jcb.200908138

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© 2009 Haynes and Silver

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 1. — Synthetic genetic toggle switches. (A) A genetic toggle switch comprised of two genes (Repressor A and Repressor B) encoding repressor proteins (RA and RB) uses a mutual repression motif to achieve bistability. Transient exposure to Input 1 inhibits RB and switches the system’s stable state to Repressor A expression. Input 2 inhibits RA and activates Repressor B and a detectable output (Reporter). (B) Stable GFP output from a synthetic prokaryotic toggle switch is activated by isopropyl-β-d-thiogalactopyranoside (IPTG) and deactivated by anhydrotetracycline (aTc; Gardner et al., 2000). The LacI and TetR repressor proteins bind the P_trc-2 and P_LtetO-1 promoters, respectively. (C) In the mammalian toggle switch, secreted alkaline phosphatase (SEAP) output is activated erythromycin (EM) and deactivated by pristinamycin I (PI; Kramer et al., 2004). Repressor proteins, containing the KRAB (Kruppel-associated box) transcription repression domain fused with either the pristinamycin-induced transcription regulator protein (PIP) or the macrolide responsive MphR(A) protein (E) bind to promoters containing a simian virus 40 region (P_SV40) and target sequences for PIP (PIR) or E (ETR).