Apical dominance

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Abstract

Apical dominance is the control exerted by the apical portions of the shoot over the outgrowth of the lateral buds. The classical explanations for correlative inhibition have focused on hormone/nutrient hypotheses. The remarkable progress that has been made in the technology of endogenous hormone quantification in plant tissue has not been accompanied by comparable progress in the elucidation of mechanisms of hormone action in apical dominance. Evidence from hormonal studies suggests that apically produced auxin indirectly suppresses axillary bud outgrowth that is promoted by cytokinin originating from roots/shoots. Significant involvement with other hormones, although less likely, has not been ruled out. Possible changes in tissue sensitivity to hormones should not be overlooked. Auxin-induced oligosaccharide signals originating from the cell walls of shoot tips or polyamines may function as secondary inhibitors to bud growth. Alternatively, apically produced auxin may suppress lateral bud growth by inhibiting auxin export from these buds. Support for a critical role for nutrients in apical dominance keeps resurfacing, especially for auxin-directed nutrient transport and for water as a possible inducing signal for bud outgrowth. Histological and biochemical analyses of lateral buds recently released from apical dominance are urgently needed. The feasibility of manipulating endogenous auxin/cytokinin content in plant tissue by gene insertion and modulation opens the door to exciting approaches as does the use of hormone insensitive/resistant mutants. There is also need to recognize the existence of variability of apical dominance mechanisms among different plant types. The aesthetic and economic implications of understanding apical dominance for the modification of plant structure and form are extremely significant. © 1991, The New York Botanical Garden. All rights reserved.

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APA

Cline, M. G. (1991). Apical dominance. The Botanical Review, 57(4), 318–358. https://doi.org/10.1007/BF02858771

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