A carotenoid-derived hormonal signal that inhibits shoot branching in plants has long escaped identification. Strigolactones are compounds thought to be derived from carotenoids and are known to trigger the germination of parasitic plant seeds and stimulate symbiotic fungi. Here we present evidence that carotenoid cleavage dioxygenase 8 shoot branching mutants of pea are strigolactone deficient and that strigolactone application restores the wild-type branching phenotype to ccd8 mutants. Moreover, we show that other branching mutants previously characterized as lacking a response to the branching inhibition signal also lack strigolactone response, and are not deficient in strigolactones. These responses are conserved in Arabidopsis. In agreement with the expected properties of the hormonal signal, exogenous strigolactone can be transported in shoots and act at low concentrations. We suggest that endogenous strigolactones or related compounds inhibit shoot branching in plants. Furthermore, ccd8 mutants demonstrate the diverse effects of strigolactones in shoot branching, mycorrhizal symbiosis and parasitic weed interaction.

Smoke is an important abiotic cue for plant regeneration in postfire landscapes. Karrikins are a class of compounds discovered in smoke that promote seed germination and influence early development of many plants by an unknown mechanism. A genetic screen for karrikin-insensitive mutants in Arabidopsis thaliana revealed that karrikin signaling requires the F-box protein MAX2, which also mediates responses to the structurally-related strigolactone family of phytohormones. Karrikins and the synthetic strigolactone GR24 trigger similar effects on seed germination, seedling photomorphogenesis, and expression of a small set of genes during these developmental stages. Karrikins also repress MAX4 and IAA1 transcripts, which show negative feedback regulation by strigolactone. We demonstrate that all of these common responses are abolished in max2 mutants. Unlike strigolactones, however, karrikins do not inhibit shoot branching in Arabidopsis or pea, indicating that plants can distinguish between these signals. These results suggest that a MAX2-dependent signal transduction mechanism was adapted to mediate responses to two chemical cues with distinct roles in plant ecology and development.

Cytokinin (CK) has long been implicated as a promoter of bud outgrowth in plants, but exactly how this is achieved in coordination with other plant hormones is unclear. The recent discovery of strigolactones (SLs) as the long-sought branchinhibiting hormone allowed us to test how CK and SL coordinately regulate bud outgrowth in pea (Pisum sativum). We found that SL-deficient plants are more sensitive to stimulation of bud growth by low concentrations of locally applied CK than wildtype plants. Furthermore, in contrast with SL mutant plants, buds of wild-type plants are almost completely resistant to stimulation by CK supplied to the vasculature. Regardless of whether the exogenous hormones were supplied locally or to the xylem stream, SL and CK acted antagonistically on bud outgrowth. These data suggest that SLs do not affect the delivery of CK to axillary buds and vice versa. Rather, these data combined with dose-response experiments suggest that SLs and CK can act directly in buds to control their outgrowth. These hormones may converge at a common point in the bud outgrowth regulatory pathway. The expression of pea BRANCHED1, a TCP transcription factor expressed strongly in buds and thought to act downstream of SLs in shoot branching, is regulated by CK and SL without a requirement for protein synthesis and in a manner that correlates with observed bud growth responses.Shoot branching is a major determinant of plant shoot architecture. Many factors contribute to the ability of an axillary bud to grow out to form a branch, including developmental, positional, genetic, hormonal, and environmental factors. Auxin, cytokinin (CK), and strigolactones (SLs) are implicated in the hormonal regulation of bud outgrowth; auxin and SLs as inhibitors of bud outgrowth and CK as a promoter of bud outgrowth (Dun et al., 2009a;Leyser, 2009;Beveridge and Kyozuka, 2010). Many studies over a number of decades have investigated the antagonistic action of auxin and CK in bud outgrowth control (ShimizuSato et al., 2009) and, more recently, the relationships between auxin and SL (Brewer et al., 2009;Crawford et al., 2010;Liang et al., 2010), but how SL and CK integrate to antagonistically control bud outgrowth remains unclear.Prior to their identification as hormones involved in shoot branching, certain properties of SLs were characterized based on studies of the long-distance branchinhibiting signal in a series of increased branching mutants. These mutants include ramosus (rms) in pea (Pisum sativum), more axillary growth (max) in Arabidopsis (Arabidopsis thaliana), decreased apical dominance (dad) in Petunia hybrida, and dwarf (d) and high tillering dwarf (htd) in rice (Oryza sativa; for review, see Dun et al., 2009a;Beveridge and Kyozuka, 2010;Domagalska and Leyser, 2011). Grafting studies demonstrated that the branch-inhibiting signal can be synthesized in root or shoot tissue, moves upward to inhibit bud outgrowth, and that a subset of the branching mutants are unable to synthesize the signal (now named SL synthesis mutants; rms1...