Abstract
Apical dominance is one of the fundamental developmental phenomena in plant biology, which determines the overall architecture of aerial plant parts. Here we show apex decapitation activated competition for dominance in adjacent upper and lower axillary buds. A two-nodal-bud pea (Pisum sativum L.) was used as a model system to monitor and assess auxin flow, auxin transport channels, and dormancy and initiation status of axillary buds. Auxin flow was manipulated by lateral stem wounds or chemically by auxin efflux inhibitors 2,3,5-triiodobenzoic acid (TIBA), 1-N-naphtylphtalamic acid (NPA), or protein synthesis inhibitor cycloheximide (CHX) treatments, which served to interfere with axillary bud competition. Redirecting auxin flow to different points influenced which bud formed the outgrowing and dominant shoot. The obtained results proved that competition between upper and lower axillary buds as secondary auxin sources is based on the same auxin canalization principle that operates between the shoot apex and axillary bud.
Highlights
One of the possibilities how to explain this behaviour of auxin is the competitive canalization model[8,9,10,11]
In plants with strong apical dominance, the shoot apex supplies the primary stem with auxin, and inhibits outgrowth of axillary buds
Saturated polar auxin flow in the primary stem does not become a sink for auxin flux from axillary buds, PIN auxin efflux carriers in buds remained unpolarized
Summary
One of the possibilities how to explain this behaviour of auxin is the competitive canalization model[8,9,10,11]. The transport narrowed to cell files, canals, where the hormone moved very effectively from source to sink These auxin transport channels subsequently patterned a new plant vasculature[12]. This concept was applied to bud outgrowth regulation: forming effective auxin transport channels from dormant axillary buds to the primary stem auxin flow was a prerequisite for its outgrowth. This in the presence of a strong auxin source–the primary SAM that supplied auxin to the primary stem and reduced its sink strength for possible secondary auxin sources–was disabled[12]. We tested the importance of long-range auxin signalling mediating bud outgrowth
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