Fig. 3: PYR1-based sensors are portable to diverse CID-based output systems demonstrated with PYR1^WIN.

a, Phosphatase inhibition. Ligand-dependent inhibition of ΔN-HAB1 phosphatase activity by recombinant receptors using a fluorogenic substrate. Inhibition expressed relative to mock controls (n = 3). b, Gene activation. Ligand-induced gene activation in S. cerevisiae using an engineered Z4-PYR1/VP64-ΔN-HAB1 genetic circuit. Whole-cell fluorescence generated from an integrated Z4₄-CYC1core-GFP-CYC1t reporter is shown (12 h after ligand addition; n = 3). c, Split luciferase complementation. Addition of ligand results in luminescence from NLuc^N-PYR1/NLuc^C-ΔN-HAB1 (n = 3). d, PYR1 ELISA-like immunoassays. Immobilized receptors recruit biotinylated ΔN-HAB1^T+ in response to ligand, and colorimetric signal is generated by a secondary streptavidin-HRP conjugate. Assays conducted in fivefold dilutions of saliva, urine, serum and blank saline are shown, with the lower limit of detection (LOD; Methods) of each assay shown (n = 3). Data points represent the mean, and the 95% confidence interval is shown on fits in a–d as gray shading and stated in square brackets along with the EC₅₀ values. e, Receptor cross-reactivity evaluation in PYR1 ELISAs. The cannabinoids shown were assayed for signal generation at 2 µM. + CNTRL, PYR1^M tested with 2 µM ABA (n = 3); RLU, relative luminescence unit. Protein parts: DBD, DNA binding domain; AD, activation domain; MBP, maltose binding protein; SA, streptavidin. Chemicals: THC, tetrahydrocannabinol; WIN, (+)-WIN 55,212-2.

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