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Our findings do not exclude a positive role for endosomal signaling or -arrestin-1 recruitment in acute responses to physiological GLP-1, but highlight how the kinetic context must be taken into account when exploiting noncanonical pathways during drug development

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We propose that removal of these key FBF partners drives the transition from a nave to a primed state ( Fig 7C, middle) , and that loss of SYGL-1 and LST-1 triggers entry into a primed state by releasing gld-1 and likely other RNAs from repression ( Fig 7C, right )