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一种共同的机制控制着植物的生命周期和结构。

A common mechanism controls the life cycle and architecture of plants.

作者信息

Ratcliffe O J, Amaya I, Vincent C A, Rothstein S, Carpenter R, Coen E S, Bradley D J

机构信息

Genetics Department, John Innes Centre, Norwich, UK.

出版信息

Development. 1998 May;125(9):1609-15. doi: 10.1242/dev.125.9.1609.

DOI:10.1242/dev.125.9.1609
PMID:9521899
Abstract

The overall aerial architecture of flowering plants depends on a group of meristematic cells in the shoot apex. We demonstrate that the Arabidopsis TERMINAL FLOWER 1 gene has a unified effect on the rate of progression of the shoot apex through different developmental phases. In transgenic Arabidopsis plants which ectopically express TERMINAL FLOWER 1, both the vegetative and reproductive phases are greatly extended. As a consequence, these plants exhibit dramatic changes in their overall morphology, producing an enlarged vegetative rosette of leaves, followed by a highly branched inflorescence which eventually forms normal flowers. Activity of the floral meristem identity genes LEAFY and APETALA 1 is not directly inhibited by TERMINAL FLOWER 1, but their upregulation is markedly delayed compared to wild-type controls. These phenotypic and molecular effects complement those observed in the tfl1 mutant, where all phases are shortened. The results suggest that TERMINAL FLOWER 1 participates in a common mechanism underlying major shoot apical phase transitions, rather than there being unrelated mechanisms which regulate each specific transition during the life cycle.

摘要

开花植物的整体地上结构取决于茎尖的一群分生细胞。我们证明,拟南芥的TERMINAL FLOWER 1基因对茎尖在不同发育阶段的发育进程速率具有统一作用。在异位表达TERMINAL FLOWER 1的转基因拟南芥植株中,营养期和生殖期都大大延长。因此,这些植株的整体形态发生了显著变化,形成了一个扩大的营养叶莲座丛,随后是一个高度分支的花序,最终形成正常的花。花分生组织特性基因LEAFY和APETALA 1的活性并未被TERMINAL FLOWER 1直接抑制,但与野生型对照相比,它们的上调明显延迟。这些表型和分子效应与在tfl1突变体中观察到的效应互补,在tfl1突变体中所有阶段都缩短。结果表明,TERMINAL FLOWER 1参与了茎尖主要阶段转变的共同机制,而不是存在调节生命周期中每个特定转变的不相关机制。

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A common mechanism controls the life cycle and architecture of plants.一种共同的机制控制着植物的生命周期和结构。
Development. 1998 May;125(9):1609-15. doi: 10.1242/dev.125.9.1609.
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