Divergent architecture of shoot models in flowering plants reflects the pattern of production of vegetative and reproductive organs from the apical meristem. The SELF-PRUNING (SP) gene of tomato is a member of a novel CETS family of regulatory genes (CEN, TFL1, and FT) that controls this process. We have identified and describe here several proteins that interact with SP (SIPs) and with its homologs from other species: a NIMA-like kinase (SPAK), a bZIP factor, a novel 10-kD protein, and 14-3-3 isoforms. SPAK, by analogy with Raf1, has two potential binding sites for 14-3-3 proteins, one of which is shared with SP. Surprisingly, overexpression of 14-3-3 proteins partially ameliorates the effect of the sp mutation. Analysis of the binding potential of chosen mutant SP variants, in relation to conformational features known to be conserved in this new family of regulatory proteins, suggests that associations with other proteins are required for the biological function of SP and that ligand binding and protein-protein association domains of SP may be separated. We suggest that CETS genes encode a family of modulator proteins with the potential to interact with a variety of signaling proteins in a manner analogous to that of 14-3-3 proteins.

The systemic model for floral induction, dubbed florigen, was conceived in photoperiod-sensitive plants but implies, in its ultimate form, a graft-transmissible signal that, although activated by different stimuli in different flowering systems, is common to all plants. We show that SFT (SINGLE-FLOWER TRUSS), the tomato ortholog of FLOWERING LOCUS T (FT), induces flowering in day-neutral tomato and tobacco plants and is encoded by SFT. sft tomato mutant plants are late-flowering, with altered architecture and flower morphology. SFT-dependent graft-transmissible signals complement all developmental defects in sft plants and substitute for long-day stimuli in Arabidopsis, short-day stimuli in Maryland Mammoth tobacco, and light-dose requirements in tomato uniflora mutant plants. The absence of donor SFT RNA from flowering receptor shoots and the localization of the protein in leaf nuclei implicate florigen-like messages in tomato as a downstream pathway triggered by cell-autonomous SFT RNA transcripts. Flowering in tomato is synonymous with termination of the shoot apical meristems, and systemic SFT messages attenuate the growth of apical meristems before and independent of floral production. Floral enhancement by systemic SFT signals is therefore one pleiotropic effect of FT orthologs.

Naturally occurring genetic variation in the universal florigen flowering pathway has produced major advancements in crop domestication. However, variants that can maximize crop yields may not exist in natural populations. Here we show that tomato productivity can be fine-tuned and optimized by exploiting combinations of selected mutations in multiple florigen pathway components. By screening for chemically induced mutations that suppress the bushy, determinate growth habit of field tomatoes, we isolated a new weak allele of the florigen gene SINGLE FLOWER TRUSS (SFT) and two mutations affecting a bZIP transcription factor component of the 'florigen activation complex' (ref. 11). By combining heterozygous mutations, we pinpointed an optimal balance of flowering signals, resulting in a new partially determinate architecture that translated to maximum yields. We propose that harnessing mutations in the florigen pathway to customize plant architecture and flower production offers a broad toolkit to boost crop productivity.