Abscisic acid (ABA) stabilizes a complex between soluble ABA receptors and downstream phosphatases; the ABA-induced complex inhibits phosphatase activity, which in turn derepresses downstream kinases and activates signaling. I will describe my lab’s work on this sensing module, our efforts to design synthetic ABA receptor agonists and antagonists, and our development of engineered signaling modules. Specifically, I will describe a potent new ABA receptor antagonist antabactin (ANT) developed using click chemistry to diversify an azide-derivative of the recently described agonist opabactin. A PYL10-ANT structure reveals that ANT occupies both the 3’ and 4’-tunnels in ABA receptor and disrupts receptor-PP2C interactions. We show that ANT treatments promote seed germination, lower leaf temperature, phenocopy the Arabidopsis abi1 mutation, and disrupt ABA-mediated transcriptional responses induced by osmotic stress. Our data also show that the previously described antagonist AA1 does not possess measurable ABA receptor antagonism. I will additionally describe a PYR1/PP2C-derived chemical-induced dimerization module that is insulated from endogenous signaling components due to surface mutations that establish an orthogonal PYR1-PP2C interaction. This engineered dimerization module provides a simple platform technology for programming crops with agrochemical-controlled traits; experiments using this module to agrochemiclally control flowering time in citrus will be described.