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The  TP53  gene fulfills a central role in protecting cells from genetic insult. Given this crucial role it might be surprising that p53 itself is not essential for cell survival. Indeed,  TP53  is the single most mutated gene across different cancer types. Thus, both a theoretical and a question of significant practical applicability arise: can cells be programmed to make  TP53  an essential gene? Here we present a genetic p53 sensor, in which the loss of p53 is coupled to the rise of  HSV-TK  expression. We show that the sensor can distinguish both p53 knockout and cells expressing a common  TP53  cancer mutation from otherwise isogenic  TP53  wild-type cells. Importantly, the system is sensitive enough to specifically target  TP53  loss-of-function cells with the HSV-TK pro-drug Ganciclovir both in vitro and in vivo. Our work opens new ways to programming cell intrinsic transformation protection systems that rely on endogenous components.

Development of a genetic sensor that eliminates p53 deficient cells