Minisymposium 27: Growth & Vegetative Development

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Abs # M2701: AtMYB2 inhibits branching by controlling cytokinin production in Arabidopsis: a post-apical dominance mechanism

Presenter:	Gan, Su-Sheng       Contact Presenter
Authors	Guo, Yongfeng  (A)   Gan, Su-Sheng  (A)
Affiliations:	(A): Cornell University

Axillary buds are groups of small SAM-like cells located in leaf axils. Outgrowth of the buds leads to branching. In order for a monocarpic plant to complete its life cycle, the axillary buds need to be suppressed permanently. The axillary buds are generally inhibited by SAM-produced auxin, which is known as apical dominance. But the apical dominance cannot suppress the axillary buds permanently because, when the main SAM becomes arrested or senescent, the apical dominance disappears. Here we report an AtMYB2-regulated post-apical dominance mechanism by which the less-branched monocarpic Arabidopsis inhibits the axillary buds from outgrowth to facilitate whole plant senescence. AtMYB2 is expressed in the compressed basal internode region of Arabidopsis at a very late stage (approximately the time when the main SAM is arrested) to suppressed the expression of the key cytokinin-synthesizing enzyme isopentenyltransferases. Cytokinins appear to be required for the outgrowth of the axillary buds. Two atmyb2 knockout lines contain higher levels of cytokinins and display a very bushy phenotype (with more than 1000 branches). Intact AtMYB2 complements the knockouts. More importantly, when the AtMYB2 promoter is used to direct AtCKX1 (a gene that encode an Arabidopsis cytokinin oxidase) in the atmyb2 null plants, the endogenous cytokinin levels are reduced to below those in WT and the mutant bushy phenotype is restored to WT, strongly suggesting that the elevated cytokinin production in atmyb2 causes the bushy phenotype by promoting the axillary bud growth.