In C. elegans, ligand binding to the LIN-12 (Notch) receptor releases the intracellular domain to activate gene transcription, together with co-effector LAG-1 (CSL). Iva Greenwald and colleagues now reveal autoregulatory mechanisms for LAG-1 that act during the development of the reproductive system. Using genome engineering methods, the researchers fluorescently label endogenous LAG-1 and observe that it is upregulated in cells in which LIN-12 signalling is active. Indeed, ectopic activation of LIN-12 increases lag-1 expression, whereas global or localised loss of LIN-12 activity decreases lag-1 expression. The authors create an endogenous synthetic operon to show that upregulation is at the level of transcription, and transgenic methods to identify an enhancer that recapitulates lag-1 expression, embedded within a LAG-1 binding site (LBS)-rich, high occupancy target (HOT) region. Mutation of LBSs disrupts lag-1 expression pattern, indicating an autoregulatory mechanism maintains lag-1 expression in cells with LIN-12 activity. Finally, deletion of the endogenous HOT region does not cause hallmark cell fate transformation, but does cause abnormal vulval development and egg-laying defects, indicating that it is required for somatic reproductive system development. Together, these data suggest that positive transcriptional autoregulation of LAG-1 contributes to the robustness of somatic reproductive system development.