Brewer Philip B, Dun Elizabeth A, Ferguson Brett J, Rameau Catherine, Beveridge Christine A
University of Queensland, Australian Research Council Centre of Excellence for Integrative Legume Research and School of Biological Sciences, St. Lucia, Queensland 4072, Australia.
Plant Physiol. 2009 May;150(1):482-93. doi: 10.1104/pp.108.134783. Epub 2009 Mar 25.
During the last century, two key hypotheses have been proposed to explain apical dominance in plants: auxin promotes the production of a second messenger that moves up into buds to repress their outgrowth, and auxin saturation in the stem inhibits auxin transport from buds, thereby inhibiting bud outgrowth. The recent discovery of strigolactone as the novel shoot-branching inhibitor allowed us to test its mode of action in relation to these hypotheses. We found that exogenously applied strigolactone inhibited bud outgrowth in pea (Pisum sativum) even when auxin was depleted after decapitation. We also found that strigolactone application reduced branching in Arabidopsis (Arabidopsis thaliana) auxin response mutants, suggesting that auxin may act through strigolactones to facilitate apical dominance. Moreover, strigolactone application to tiny buds of mutant or decapitated pea plants rapidly stopped outgrowth, in contrast to applying N-1-naphthylphthalamic acid (NPA), an auxin transport inhibitor, which significantly slowed growth only after several days. Whereas strigolactone or NPA applied to growing buds reduced bud length, only NPA blocked auxin transport in the bud. Wild-type and strigolactone biosynthesis mutant pea and Arabidopsis shoots were capable of instantly transporting additional amounts of auxin in excess of endogenous levels, contrary to predictions of auxin transport models. These data suggest that strigolactone does not act primarily by affecting auxin transport from buds. Rather, the primary repressor of bud outgrowth appears to be the auxin-dependent production of strigolactones.
在上个世纪,人们提出了两个关键假说来解释植物的顶端优势:生长素促进一种第二信使的产生,该信使向上移动到芽中以抑制其生长,并且茎中的生长素饱和会抑制生长素从芽中运输,从而抑制芽的生长。最近发现独脚金内酯是一种新型的侧枝生长抑制剂,这使我们能够测试其与这些假说相关的作用模式。我们发现,即使在豌豆(Pisum sativum)去顶后生长素耗尽的情况下,外源施加独脚金内酯仍能抑制芽的生长。我们还发现,在拟南芥(Arabidopsis thaliana)生长素反应突变体中施加独脚金内酯会减少分枝,这表明生长素可能通过独脚金内酯发挥作用以促进顶端优势。此外,与施加生长素运输抑制剂N-1-萘基邻苯二甲酸(NPA)不同,将独脚金内酯施加到突变或去顶豌豆植株的小芽上会迅速停止其生长,NPA只有在几天后才会显著减缓生长。虽然将独脚金内酯或NPA施加到正在生长的芽上会缩短芽的长度,但只有NPA会阻断芽中的生长素运输。野生型以及独脚金内酯生物合成突变体的豌豆和拟南芥枝条能够立即运输超过内源性水平的额外生长素,这与生长素运输模型的预测相反。这些数据表明,独脚金内酯并不主要通过影响芽中生长素的运输来发挥作用。相反,芽生长的主要抑制因子似乎是生长素依赖性的独脚金内酯产生。