Abstract
The physiology and genetics underlying juvenility is poorly understood. Here, we exploit Arabidopsis as a system to understand the mechanisms that regulate floral incompetence during juvenility. Using an experimental assay that allows the length of juvenility to be estimated and mutants impaired in different pathways, we show that multiple inputs influence juvenility. Juvenile phase lengths of wild type (WT) accessions Col-0, Ler-0 and Ws-4 are shown to differ, with Col-0 having the shortest and Ws-4 the longest length. Plants defective in sugar signalling [gin1-1, gin2-1, gin6 (abi4)] and floral repressor mutants [hst1, tfl1, tfl2 (lhp1)] showed shortened juvenile phase lengths compared to their respective WTs. Mutants defective in starch anabolism (adg1-1, pgm1) and catabolism (sex1, sex4, bam3) showed prolonged juvenile phase lengths compared to Col-0. Examination of diurnal metabolite changes in adg1-1 and sex1 mutants indicates that their altered juvenile phase length may be due to lack of starch turnover, which influences carbohydrate availability. In this article, we propose a model in which a variety of signals including floral activators and repressors modulate the juvenile-to-adult phase transition. The role of carbohydrates may be in their capacity as nutrients, osmotic regulators, signalling molecules and/ or through their interaction with phytohormonal networks.