HB21/40/53 promote inflorescence arrest through ABA accumulation at the end of flowering

Abstract

AbstractFlowers are produced by the activity of the inflorescence meristem after the floral transition. In plants with indeterminate inflorescences, as Arabidopsis, the final number of flowers produced by the inflorescence meristem will depend on two main factors, the rate of flower production by the meristem and the duration of the phase of inflorescence meristem activity. The end of flowering, understood as the moment when the inflorescence stops the production of new flowers, is associated with the meristem proliferative arrest. At this time point, the meristem ceases to initiate new floral primordia and the unpollinated flowers already formed arrest their development.It has been known for a long time that fruit/seed production induces inflorescence meristem arrest, but the mechanisms controlling this process were elusive. During the last years, the regulation of the end of flowering has started to be elucidated in Arabidopsis. The meristem arrest at the end of flowering is controlled at the genetic level by the FRUITFULL-APETALA2 (FUL-AP2) pathway, that modulates meristem activity. The meristem arrest has been also shown to be controlled at the hormonal level. It has been proposed that auxin could mediate the fruit/seed effect to the meristem. Cytokinins regulation and response have been also proposed as important factors controlling the meristem activity at the end of flowering. Finally, it has been also described that arrested meristems at the end of flowering resembles dormant meristem at the transcriptomic level.Previously, we have shown that the FUL-AP2 pathway controls the expression of the homeodomain leucine zipper transcription factorHOMEOBOX PROTEIN 21(HB21), a gene involved in the establishment of bud axillary dormancy. In this work we characterize the role ofHB21in the control of the proliferative arrest associated with the end of flowering. We observed thatHB21, together withHB40andHB53, accumulate in the inflorescence apexes at the end of flowering promoting the cessation of inflorescence meristem activity. We also show thatHB21induction of in young apexes is sufficient to induce flower and meristem arrest, likely mediated by an increase in ABA responses. Thus, our work confirms the parallelism proposed between dormant meristems and the arrested meristem at the end of flowering, which appear to be regulated by common pathways, and propose ABA as a new regulator in the control of inflorescence meristem arrest.