The urate-regulating synthetic circuit of Kemmer and colleagues [24]. A urate transporter, a urate sensitive DNA binding protein, and an engineered promoter-operator-gene complex, are introduced into cells. With no urate, the DNA-binding protein binds the operator site in the DNA and inhibits the transcription of urate oxidase. With urate present, it binds urate instead, freeing the operator and allowing the urate oxidase to be transcribed. Following translation, the enzyme destroys urate, returning the system to its starting condition. 

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... The light-sensitivity opens the door to an electro-photo-biological feedback system, in which measurements of physiology can be processed electronically and fed back to a synthetic biological effector by light. Ultimately, if would be useful to build feedback into the synthetic constructs themselves, with no need for triggering by light. This has not been done for blood sugar, but it has been done for control of blood urate by urate-triggered production of a urate oxidase [24]: the engineered system has a beneficial effect in an animal model of hyperuricemia. The synthetic system involved (Fig 3) used a urate sensor from Deinococcus and a urate oxidase from Aspergillus , and operated in mammalian cells: this cross-phylum approach is typical of contemporary synthetic biology. A few years ago, my laboratory published a speculative paper that identified single driver genes that could activate common types of morphogenetic cell behaviour: the paper sketched how these genes might be built into simple synthetic modules for 'synthetic morphology' [19]. We have now built some of these modules and have shown that they function as intended, at least at the level of cell behaviour in culture [25]. Specifically, they confer on human cells controllable proliferation, apoptosis, adhesion, locomotion and formation of syncytia. The next experimental stage is the combination of cells carrying different modules to try to produce simple artificial 'tissues', and combination of the cells with normal cells to test the possibility of their making defined, designed connections. This work remains a long way from production of practical synthetic tissues, but it may turn out to be a first step towards that goal. When stem cells are introduced into human recipients, especially after any genetic modification, there is a risk that they will behave pathologically, in particular by generating a neoplasm. One means of controlling this risk would be building a “kill switch” into the cells so that they can be eliminated by a specified externally-applied signal. Such a switch, using an inducible caspase to drive apoptosis, has already been built and tested in an experimental clinical trial in the field of immunology [26]. Clearly, whatever pharmacological signals are given to activate a 'kill switch' in a patient, they will have to be safe drugs. Given that clinical trials to prove the safety of drugs are so expensive, ...