Auxin export from proximal fruits drives arrest in competent inflorescence meristems

Abstract

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.

SMALL LEAF AND BUSHY1 controls organ size and lateral branching by modulating the stability of BIG SEEDS1 in Medicago truncatula

“…The phytohormones auxin and cytokinin have long been implicated in the process, in which auxin inhibited the outgrowth of axillary buds by affecting the supply of cytokinin to axillary buds (Eklof et al , ; Li & Bangerth, ; Nordstrom et al , ; Tanaka et al , ). Notably, many flowering plants with sterility issues exhibited increased branching, which is thought to be an indirect effect of the auxin export levels from growing meristems vs fruits (Hensel et al , ; Ware et al , ). The observation of sterility and increased branching in the slb1 mutant suggests that the SLB1 regulation of lateral bud outgrowth may be connected to auxin transport.…”