Plant architecture and subsequent productivity are determined by the shoot apical dominance, which is disturbed by the deficiency of boron, one of the essential trace elements for plant growth and reproduction. However, the mechanism by which B controls shoot apical dominance or axillary bud outgrows under B deficiency is still unclear. This work aimed to investigate the mechanistic basis of this process, with focus on the interaction between B and polar auxin transport. Adopting an all-buds phenotyping methodology and employing several complementary approaches, we found that boron deficiency inhibited plant growth and changed the shoot architecture, resulting in the outgrowth of axillary buds at nodes 1-3. This was related to the auxin accumulation in shoot apical parts buds under B deficiency. Applying N-1-naphthylphthalamic acid to inhibit auxin transport from the shoot apex promoted the outgrowth of axillary buds in boron-sufficient (+B) plants. In decapitated plants, the application of exogenous auxin to the shoot apex only inhibited the outgrowth of axillary buds in +B plants. At higher auxin doses, the toxic effect of IAA was observed in the lower part of the shoot, which was more severe in +B plants than in B-deprived (-B) plants. Furthermore, the expression of PsPIN3 was significantly downregulated under -B conditions. These results indicate that B deficiency inhibits PAT from the apical bud through the main stem to the lower parts, leading to an increase of auxin level in the apical bud, which inhibits the growth of apical buds while stimulating the outgrowth of axillary buds.
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