The role of Strigolactone and KAI2 signalling in seedling development

Strigolactones (SL) and the endogenous KAI2-ligand (KL) are butenolide compounds acting as hormonal signals to regulate multiple aspects of plant development and architecture. Perception of these signals in Arabidopsis thaliana requires respectively DWARF14 (D14) and KARRIKIN INSENSITIVE 2 (KAI2) receptors and the shared F-box protein MAX2. The MAX2-mediated ubiquitination and subsequent degradation of SUPPRESSOR OF MAX2 1 (SMAX1), SMAX1-like 2 (SMXL2), or their homologues SMXL6, SMXL7, and SMXL8 triggers the downstream effects of KL or SL signalling. SL signalling is a potent regulator of shoot architecture and increase in SL biosynthesis is linked with the plant response to nutrients depletion. The regulation of root development by SL signalling has also been proposed, although it remains elusive given it is mainly based on the use of max2 mutant and rac-GR24 treatments, both acting indiscriminately in SL and KL signalling. The exact functions of SMXL6, 7, and 8 are not yet fully understood, but it is clear that D14-mediated strigolactone signalling pathway regulates auxin distribution by re-modelling auxin transport in the shoot. Despite considerable interest in its function, the role of KAI2 and its proteolytic targets SMAX1/SMXL2 in seedling development remains poorly understood. KAI2 signalling is required for a normal photomorphogenetic development of the seedlings, such as hypocotyl growth and germination, but it is yet unknown if KAI2 also accounts for some aspects of the MAX2-mediated root development.
The close origins between SL and KAI2 signalling pathways prompted us to reassess the role of SL and KL signalling in root development by phenotyping mutants affected in both pathways. My results indicate a dual role of SL and KL in root development. SL signalling promotes primary root growth, and KAI2 signalling is a newly discovered important regulator of the lateral root and root hair development. I demonstrated that the strong phenotypes of kai2 are correlated with altered auxin sensitivity in roots.
Given both pathways appear to regulate physiological processes in the root and seedlings, I investigated if either the functions of SL and/or KL signalling in seedling development were associated with environmental stress responses. I found that KL and SL signalling are required for the correct developmental adaption in response to low phosphorus availability; and KAI2 and SMAX1/SMXL2 modulate root hair and lateral root proliferation consequently. In addition, I showed that KAI2 signalling is required for the correct photomorphogenic remodelling of seedling growth, and that kai2 and smax1 smxl2 mutants display a range of phenotypic traits and atypical adaptive responses associated with defect in auxin biosynthesis/response.
Following a detailed analysis of the KAI2-mediated photomorphogenic remodelling, I demonstrated that KAI2 control the light-induced remodelling of PIN-mediated auxin transport system. Although the exact mechanisms remain unclear, I showed that KAI2 is required for appropriate changes in PIN protein abundance at the plasma membrane in various tissues affected by light-remodelling.