Roles for Auxin, Cytokinin, and Strigolactone in Regulating Shoot Branching

Roles for Auxin, Cytokinin, and Strigolactone in Regulating Shoot Branching
复制标题

DOI:
10.1104/pp.109.135475
复制
发表时间:
2009-04-01
期刊:
影响因子:
7.4
通讯作者:
Beveridge, Christine A.
Beveridge, Christine A.
中科院分区:
生物学1区
文献类型:
--
作者:
Ferguson, Brett J.;Beveridge, Christine A.

文献摘要

被引文献

相似文献

许多过程已被描述在控制枝条分枝。顶端优势是指茎尖对腋芽生长的控制作用,而相关抑制则包括对其他生长芽或枝条生长的抑制作用。植物激素生长素在茎和芽中的水平、信号和/或流动被认为参与了这些过程。此外,豌豆(Pisum sativum)中的RAMOSUS(RMS)分支基因控制茎和根中产生的长距离抑制性分支信号、独脚金内酯或产物的合成和感知。生长素处理影响RMS基因的表达,但目前还不清楚RMS网络是否可以独立于生长素调节分支。在这里,我们探讨顶端优势和相关抑制是否表现出独立的或加性的RMS突变体植物的影响。与完整的对照植株相比,去头和茎环的rms突变体的芽生长和分支长度得到增强。这可能与这些处理不依赖RMS诱导腋芽生长有关。RMS突变体植物中的相关抑制也很明显,再次表明RMS独立的组件。降低RMS 1和RMS 5基因表达、生长素运输和主茎生长素水平的处理并不总是足以促进芽的生长。我们认为,这可能与未能诱导细胞分裂素生物合成基因的表达,这总是与芽生长在我们的治疗。我们提出了一个新的模型,该模型解释了顶端优势、相关抑制、RMS基因作用、生长素和细胞分裂素及其相互作用,通过从休眠到持续生长的不同控制点控制芽的进展。
Many processes have been described in the control of shoot branching. Apical dominance is defined as the control exerted by the shoot tip on the outgrowth of axillary buds, whereas correlative inhibition includes the suppression of growth by other growing buds or shoots. The level, signaling, and/or flow of the plant hormone auxin in stems and buds is thought to be involved in these processes. In addition, RAMOSUS (RMS) branching genes in pea (Pisum sativum) control the synthesis and perception of a long-distance inhibitory branching signal produced in the stem and roots, a strigolactone or product. Auxin treatment affects the expression of RMS genes, but it is unclear whether the RMS network can regulate branching independently of auxin. Here, we explore whether apical dominance and correlative inhibition show independent or additive effects in rms mutant plants. Bud outgrowth and branch lengths are enhanced in decapitated and stem-girdled rms mutants compared with intact control plants. This may relate to an RMS-independent induction of axillary bud outgrowth by these treatments. Correlative inhibition was also apparent in rms mutant plants, again indicating an RMS-independent component. Treatments giving reductions in RMS1 and RMS5 gene expression, auxin transport, and auxin level in the main stem were not always sufficient to promote bud outgrowth. We suggest that this may relate to a failure to induce the expression of cytokinin biosynthesis genes, which always correlated with bud outgrowth in our treatments. We present a new model that accounts for apical dominance, correlative inhibition, RMS gene action, and auxin and cytokinin and their interactions in controlling the progression of buds through different control points from dormancy to sustained growth.