A well-defined set of regulatory pathways control entry into the reproductive phase in flowering plants [1]. Conversely, little is known about the mechanisms that control the end of the reproductive phase ('floral arrest'), despite this being a critical process for optimising fruit and seed production. Complete fruit removal or lack of fertile fruit-set in male sterile mutants, for example male sterile1 (ms1), prevents timely floral arrest in the model plant Arabidopsis [2]. These observations formed the basis for Hensel and colleagues' model in which end-of-flowering was proposed to result from a cumulative fruit/seed-derived signal that caused simultaneous 'global proliferative arrest' (GPA) in all inflorescences [2]. Recent studies have suggested that end-of-flowering involves gene expression changes at the floral meristem which are at least in part controlled by the FRUITFULL-APETELA2 pathway [3,4], however there is limited understanding of how this process is controlled and the communication needed at the whole plant level. Here, we provide new information providing a framework for the fruit-to-meristem (F-M) communication implied by the GPA model [5]. We show that floral arrest in Arabidopsis is not 'global' and does not occur synchronously between branches, but rather that the arrest of each inflorescence is a local process, driven by auxin export from fruit proximal to the inflorescence meristem (IM). Furthermore, we show that inflorescence meristems are only competent for floral arrest once they reach a certain developmental age. Understanding the regulation of floral arrest is of major importance for the future manipulation of flowering to extend and maximise crop yields.