Background Strigolactones (SLs) are an important class of carotenoid-derived signalling molecule in plants, which function both as exogenous signals in the rhizosphere and as endogenous plant hormones. In flowering plants, SLs are synthesized by a core pathway of four enzymes and are perceived by the DWARF14 (D14) receptor, leading to degradation of SMAX1-LIKE7 (SMXL7) target proteins in a manner dependent on the SCF MAX2 ubiquitin ligase. The evolutionary history of SLs is poorly understood, and it is not clear whether SL synthesis and signalling are present in all land plant lineages, nor when these traits evolved. Results We have utilized recently-generated genomic and transcriptomic sequences from across the land plant clade to resolve the origin of each known component of SL synthesis and signalling. We show that all enzymes in the core SL synthesis pathway originated at or before the base of land plants, consistent with the previously observed distribution of SLs themselves in land plant lineages. We also show that the late-acting enzyme LATERAL BRANCHING OXIDOREDUCTASE (LBO) may be considerably more ancient than previously thought. We perform a detailed phylogenetic analysis of SMXL proteins and show that specific SL target proteins only arose in flowering plants. We also assess diversity and protein structure in the SMXL family, identifying several previously unknown clades. Conclusions Overall, our results suggest that SL synthesis is much more ancient than canonical SL signalling, consistent with the idea that SLs first evolved as rhizosphere signals and were only recruited much later as hormonal signals. Electronic supplementary material The online version of this article (10.1186/s12915-019-0689-6) contains supplementary material, which is available to authorized users.

A well-defined set of regulatory pathways control entry into the reproductive phase in flowering plants. 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, prevents timely floral arrest in the model plant Arabidopsis, leading to a previous proposal that floral arrest results from a cumulative fruit/seed-derived signal that causes simultaneous 'global proliferative arrest' (GPA).Recent studies have suggested that floral arrest involves gene expression changes in the inflorescence meristem that are at least in part controlled by the FRUITFULL-APETALA2 pathway, however there is limited understanding of how this process is controlled and the communication needed at the whole plant level. Here, we provide a framework for the communication previously inferred in the GPA model. 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 apex. Furthermore, we show that inflorescences 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.

Floral morphology determines the pattern of pollen transfer within and between individuals. In hermaphroditic species, the spatial arrangement of sexual organs influences the rate of self-pollination as well as the placement of pollen in different areas of the pollinator's body. Studying the evolutionary modification of floral morphology in closely related species offers an opportunity to investigate the causes and consequences of floral variation. Here, we investigate the recurrent modification of flower morphology in three closely related pairs of taxa in Solanum section Androceras (Solanaceae), a group characterized by the presence of two morphologically distinct types of anthers in the same flower (heteranthery). We use morphometric analyses of plants grown in a common garden to characterize and compare the changes in floral morphology observed in parallel evolutionary transitions from relatively larger to smaller flowers. Our results indicate that the transition to smaller flowers is associated with a reduction in the spatial separation of anthers and stigma, changes in the allometric relationships among floral traits, shifts in pollen allocation to the two anther morphs and reduced pollen : ovule ratios. We suggest that floral modification in this group reflects parallel evolution towards increased self-fertilization and discuss potential selective scenarios that may favour this recurrent shift in floral morphology and function.

Plants continually integrate environmental information to make decisions about their development. Correlative controls, in which one part of the plant regulates the growth of another, form an important class of regulatory mechanism, but their study has been neglected and their molecular basis remains unclear. In this review, we examine the role of negative correlative controls or 'dominance' phenomena in the regulation of shoot architecture. Apical dominance, in which actively growing shoot branches inhibit the growth of other branches, is perhaps the most famous example of this. We discuss the recent progress made in understanding the mechanistic basis for apical dominance, and three plausible models for shoot branching control. We then use the apical dominance paradigm to explore other dominance phenomena, including seed-seed inhibition (carpic dominance), seed-tomeristem inhibition, and the control of maternal senescence by seeds. We propose that apical and carpic dominance may share a common mechanistic basis rooted in auxin transport canalization. Conversely, we conclude that seed-to-meristem inhibition and seed-driven senescence may not be 'true' correlative controls, but rather more complex phenomena in which seed-set plays a permissive rather than instructive role. Overall, we attempt to develop a coherent framework for understanding the developmental and regulatory mechanisms that control shoot architecture, and provide new insights into the end of flowering, fruiting and growth.

Hypocotyl phototropism of etiolated Arabidopsis seedlings is primarily mediated by the blue-light receptor kinase phototropin 1 (phot1). Phot1-mediated curvature to continuous unilateral blue light irradiation (0.5 μmol m−2 s−1) is enhanced by overhead pre-treatment with red light (20 μmol m−2 s−1 for 15 min) through the action of phytochrome (phyA). Here, we show that pre-treatment with blue light is equally as effective in eliciting phototropic enhancement and is dependent on phyA. Although blue light pre-treatment was sufficient to activate early phot1 signaling events, phot1 autophosphorylation in vivo was not found to be saturated, as assessed by subsequently measuring phot1 kinase activity in vitro. However, enhancement effects by red and blue light pre-treatment were not observed at higher intensities of phototropic stimulation (10 μmol m−2 s−1). Phototropic enhancement by red and blue light pre-treatments to 0.5 μmol m−2 s−1 unilateral blue light irradiation was also lacking in transgenic Arabidopsis where PHOT1 expression was restricted to the epidermis. Together, these findings indicate that phyA-mediated effects on phot1 signaling are restricted to low intensities of phototropic stimulation and originate from tissues other than the epidermis.