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The role of auxin transport in bud activation

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An important component of plant architecture is the degree of shoot branching. This is an example of phenotypic plasticity, whereby plants change their development in response to its environment. The outgrowth of branches is influenced, for example, by light, nutrients and planting density as well as the developmental stage of the plant. Recent evidence indicates that bud activation is initiated by canalized auxin transport from the bud to the main stem giving rise to a systemic control mechanism. Additionally, the phytohormones strigolactone (SL) and cytokinin (CK) inhibit and promote branch outgrowth respectively and it has also been proposed that these hormones act locally as second messengers within buds to regulate outgrowth. SL and CK alter the level of the TCP transcription factor, BRANCHED 1 (BRC1) which is expressed in dormant buds, leading to the idea that BRC1 is an integrator of branching signals. It is not clear, however, whether this is a direct response to hormone signals, or a downstream effect of bud growth. To understand the role of BRC1 in more detail, I have been examining its expression levels under different bud-activating treatments as well as examining how BRC1 relates to changes in auxin transport activity. Through investigating the role of BRC1 in conjunction with the onset of bud auxin export and actual growth, I hope to build up a picture of the timing and order of events during bud activation. This will contribute to understanding whether local hormone action or auxin canalization is more important in regulating branching.

This talk is part of the Plant Sciences Research Seminars series.

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