AGO1 controls arabidopsis inflorescence architecture possibly by regulating TFL1 expression
AGO1 controls arabidopsis inflorescence architecture possibly by regulating TFL1 expression
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DOI：
10.1093/aob/mcu132
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发表时间：
2014-11-01
期刊：
影响因子：
4.2
通讯作者：
Madueno, F.
中科院分区：
文献类型：
--
作者：
Fernandez-Nohales, P.;Domenech, M. J.;Madueno, F.
TERMINAL FLOWER 1 (TFL1) 基因对于控制拟南芥花序结构至关重要。因此，tfl1突变体开花早，花序期非常短，而TFL1过表达植物的营养期和花序期延长，产生许多共花期。 TFL1 在芽分生组织中表达，而不是在花中表达。在花序顶端，TFL1 将花基因 LEAFY (LFY) 和 APETALA1 (AP1) 限制在花上，而 LFY 和 AP1 将 TFL1 限制在花序分生组织上。尽管 TFL1 在花序结构中发挥着核心作用，但对其表达的调控却知之甚少。本研究旨在通过鉴定和研究新型 TFL1 调节因子来扩大对花序发育的理解。对携带 TFL1::GUS（β-葡萄糖醛酸酶）报告基因构建体的拟南芥品系进行诱变，以分离出 TFL1 表达发生改变的突变体。通过定位克隆鉴定了突变基因。通过实时PCR和组织化学GUS检测分析TFL1和TFL1::GUS的表达。双突变体分析用于评估 TFL1 对花序突变体表型的贡献。分离出同时具有增加的共花序数量和高异位 TFL1 表达的突变体。突变基因的克隆表明，这两种表型都是由 ARGONAUTE1 (AGO1) 基因突变引起的，该基因编码 RNA 沉默机制的关键组成部分。对另一个 ago1 等位基因的分析表明，共花的增殖和异位 TFL1 表达表型不是等位基因特异性的。 ago1 tfl1 双突变体中共花数量的增加受到抑制。结果表明 AGO1 是 TFL1 表达的抑制因子。此外，他们揭示了 AGO1 在花序发育中的新作用，控制共花序的产生。 AGO1 似乎是通过调节 TFL1 表达来发挥这一作用的。
The TERMINAL FLOWER 1 (TFL1) gene is pivotal in the control of inflorescence architecture in arabidopsis. Thus, tfl1 mutants flower early and have a very short inflorescence phase, while TFL1-overexpressing plants have extended vegetative and inflorescence phases, producing many coflorescences. TFL1 is expressed in the shoot meristems, never in the flowers. In the inflorescence apex, TFL1 keeps the floral genes LEAFY (LFY) and APETALA1 (AP1) restricted to the flower, while LFY and AP1 restrict TFL1 to the inflorescence meristem. In spite of the central role of TFL1 in inflorescence architecture, regulation of its expression is poorly understood. This study aims to expand the understanding of inflorescence development by identifying and studying novel TFL1 regulators.Mutagenesis of an Arabidopsis thaliana line carrying a TFL1::GUS (beta-glucuronidase) reporter construct was used to isolate a mutant with altered TFL1 expression. The mutated gene was identified by positional cloning. Expression of TFL1 and TFL1::GUS was analysed by real-time PCR and histochemical GUS detection. Double-mutant analysis was used to assess the contribution of TFL1 to the inflorescence mutant phenotype.A mutant with both an increased number of coflorescences and high and ectopic TFL1 expression was isolated. Cloning of the mutated gene showed that both phenotypes were caused by a mutation in the ARGONAUTE1 (AGO1) gene, which encodes a key component of the RNA silencing machinery. Analysis of another ago1 allele indicated that the proliferation of coflorescences and ectopic TFL1 expression phenotypes are not allele specific. The increased number of coflorescences is suppressed in ago1 tfl1 double mutants.The results identify AGO1 as a repressor of TFL1 expression. Moreover, they reveal a novel role for AGO1 in inflorescence development, controlling the production of coflorescences. AGO1 seems to play this role through regulating TFL1 expression.