Regulatory dynamics of axillary bud competition in Arabidopsis

The branching architecture of a plant depends on the activity of its axillary buds, which are continuously produced during development. Each axillary bud can either stay dormant or activate to form a branch, giving rise to a large number of possible branching forms. Whether a bud activates depends on the integration of local signals in the bud, as well as systemic signals from across the plant. The importance of systemic regulation is exemplified by the observation that the growth of an axillary branch can inhibit the activation of buds elsewhere on the plant. This phenomenon of so-called bud-bud competition is hypothesised to be based on their competition for auxin export; bud activation is thought to depend on the ability of buds to establish canalised auxin transport from the bud into the main stem, which can be prevented by the presence of an already canalised bud. In addition to systemic regulation via auxin transport canalisation, local regulation in the bud by the transcription factor BRANCHED1 (BRC1), has an important role in maintaining bud dormancy. However, its relationship to auxin canalisation-based regulation is poorly understood. This is particularly apparent when studying the effect of strigolactone, a plant hormone which affects both BRC1 expression and the removal of the PIN1 auxin transporter from the plasma membrane. The relative influences of these two arms of strigolactone signaling is poorly understood, because they have mostly been studied separately. In this thesis, I first show that both hubs of regulation must be taken into account in order to understand the dynamics of bud competition. My results on the influence of BRC1 in bud growth dynamics are consistent with a hypothesised role for BRC1 influencing the time needed to establish canalised auxin transport from the bud into the main stem. To test this hypothesis, I build a simple canalisation based model of bud competition, which incorporates BRC1 as regulating the strength of the positive feedback on auxin transport. I find that this model captures a range of phenotypes from genetic or pharmacological perturbations of auxin transport and/or BRC1 expression. I use this model to predict the effect of strigolactone acting independently of PIN1 removal. I validate these predictions through experiments using a transgenic line bearing a strigolactone insensitive PIN1 transporter. These results support the model formulation, namely that BRC1 could act by regulating the strength of the positive feedback on canalisation. Overall, this work integrates two previously disparate models of shoot branching regulation.