Strigolactone regulates shoot development through a core signalling pathway

Strigolactones are a recently identified class of hormone that regulate multiple aspects of plant development. The DWARF14 (D14) /{beta} fold protein has been identified as a strigolactone receptor, which can act through the SCFMAX2 ubiquitin ligase, but the universality of this mechanism is not clear. Multiple proteins have been suggested as targets for strigolactone signalling, including both direct proteolytic targets of SCFMAX2, and downstream targets. However, the relevance and importance of these proteins to strigolactone signalling in many cases has not been fully established. Here we assess the contribution of these targets to strigolactone signalling in adult shoot developmental responses. We find that all examined strigolactone responses are regulated by SCFMAX2 and D14, and not by other D14-like proteins. We further show that all examined strigolactone responses likely depend on degradation of SMXL proteins in the SMXL6 clade, and not on other proposed proteolytic targets. Taken together, our results suggest that in the adult shoot, the dominant mode of strigolactone signalling is D14-initiated, MAX2-mediated degradation of SMXL6-related proteins. We confirm that the BRANCHED1 transcription factor and the PIN-FORMED1 auxin efflux carrier are plausible downstream targets of this pathway in the regulation of shoot branching, and show that BRC1 likely acts in parallel to PIN1.\n\nAUTHOR SUMMARYStrigolactones are a recently discovered family plant hormones with diverse roles in development, most strikingly in the regulation shoot branching. Our understanding of the mechanism(s) by which plants perceive and respond to strigolactones is growing rapidly. It is likely that the strigolactone signaling pathway has evolved by duplication and diversification of specific components of a pre-existing pathway, involved in perception and response to an as yet unknown hormone. Several of these components have been identified and several new candidate components have been implicated in the pathway. We have adopted a genetic approach to assess systematically the contributions of all these players to strigolactone signaling in the shoot. We exclude some of the candidate proteins from involvement in strigolactone-mediated shoot branching control and define a core pathway for strigolactone action in the shoot. We provide evidence that downstream of this core, the strigolactone signaling pathway branches, with different effectors mediating different shoot responses.