Department of Biology, Building 44, The University, SO9 5NH, Southampton, UK.
Planta. 1990 Apr;181(1):117-24. doi: 10.1007/BF00202333.
Correlatively inhibited pea shoots (Pisum sativum L.) did not transport apically applied (14)C-labelled indol-3yl-acetic acid ([(14)C]IAA), and polar IAA transport did not occur in internodal segments cut from these shoots. Polar transport in shoots and segments recovered within 24 h of removing the dominant shoot apex. Decapitation of growing shoots also resulted in the loss of polar transport in segments from internodes subtending the apex. This loss was prevented by apical applications of unlabelled IAA, or by low temperatures (approx. 2° C) after decapitation. Rates of net uptake of [(14)C]IAA by 2-mm segments cut from subordinate or decapitated shoots were the same as those in segments cut from dominant or growing shoots. In both cases net uptake was stimulated to the same extent by competing unlabelled IAA and by N-1-naphthylphthalamic acid. Uptake of the pH probe [(14)C]-5,5-dimethyloxazolidine-2,4-dione from unbuffered solutions was the same in segments from both types of shoot. Patterns of [(14)C]IAA metabolism in shoots in which polar transport had ceased were the same as those in shoots capable of polar transport. The reversible loss of polar IAA transport in these systems, therefore, was not the result of loss or inactivation of specific IAA efflux carriers, loss of ability of cells to maintain transmembrane pH gradients, or the result of a change in IAA metabolism. Furthermore, in tissues incapable of polar transport, no evidence was found for the occurrence of inhibitors of IAA uptake or efflux. Evidence is cited to support the possibility that the reversible loss of polar auxin transport is the result of a gradual randomization of effluxcarrier distribution in the plasma membrane following withdrawal of an apical auxin supply and that the recovery of polar transport involves reestablishment of effluxcarrier asymmetry under the influence of vectorial gradients in auxin concentration.
相关性抑制豌豆苗(Pisum sativum L.)不会运输顶端应用的(14)C 标记吲哚-3-乙酸([(14)C]IAA),并且从这些苗中切下的节间段也不会发生极性 IAA 运输。在去除优势苗顶后 24 小时内,苗和节段中的极性运输恢复。生长苗的去顶也导致顶端下节间段的极性运输丧失。未标记 IAA 的顶端应用或去顶后低温(约 2°C)可防止这种损失。从从属或去顶苗切下的 2mm 段的[(14)C]IAA 的净摄取率与从优势或生长苗切下的段相同。在这两种情况下,未标记 IAA 和 N-1-萘基邻苯二甲酰亚胺的竞争都以相同的程度刺激净摄取。从未缓冲溶液中摄取 pH 探针[(14)C]-5,5-二甲基恶唑烷-2,4-二酮在两种类型的苗段中是相同的。在极性运输已停止的苗中,[(14)C]IAA 代谢的模式与能够进行极性运输的苗相同。因此,在这些系统中,极性 IAA 运输的可逆丧失不是特定 IAA 外排载体的丧失或失活、细胞维持跨膜 pH 梯度的能力丧失的结果,也不是 IAA 代谢变化的结果。此外,在不能进行极性运输的组织中,没有发现 IAA 摄取或外排抑制剂的存在。引用证据支持这样一种可能性,即极性生长素运输的可逆丧失是在顶端生长素供应停止后,质膜中外排载体分布逐渐随机化的结果,并且极性运输的恢复涉及在生长素浓度的向量梯度的影响下重新建立外排载体的不对称性。