Abstract

According to the auxin-inhibition hypothesis of apical dominance, apically produced auxin moves down the stem and inhibits axillary bud outgrowth, either directly or indirectly. This hypothesis has been examined further by monitoring changes in basipetal auxin transport and endogenous auxin concentration in Ipomoea nil caused by shoot inversion, a stimulus that releases apical dominance. The results indicate that inversion reduces auxin transport in the main stem. In upright shoots of intact plants, a 16-h pretreatment with [3H]IAA 4 cm below the apex results in downward movement of label and accumulation in nodes, especially the cotyledonary node. Label does not accumulate in the lateral buds. GC-MS determinations of endogenous free auxin level in the fourth node, where a lateral bud grows out following inversion of the upper part of the shoot, show no changes at 3 and 8 h after inversion, the range of times for inversion-induced bud release, or at 24 h, when bud outgrowth is continuing. However, inversion did cause a just-detectable decrease (approx. 10%) in the IAA level of the shoot's elongation region. Although auxin transport in segments of the main stem is partially inhibited by inversion over a period shorter than the latent time of bud release, thus providing a means for the expected depletion of auxin in the fourth node, no depletion could be detected there. These results suggest that either a decrease in IAA level in the main stem is not causal of bud release or that the decreased IAA pool responsible for bud release is compartmented and cannot be measured in whole-tissue extracts.

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