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花分生组织特征基因的进化。黑麦草中与拟南芥APETALA1和LEAFY相关基因的分析。

Evolution of floral meristem identity genes. Analysis of Lolium temulentum genes related to APETALA1 and LEAFY of Arabidopsis.

作者信息

Gocal G F, King R W, Blundell C A, Schwartz O M, Andersen C H, Weigel D

机构信息

Commonwealth Scientific and Industrial Research Organization, Division of Plant Industry, G.P.O. Box 1600, Canberra, ACT 2601, Australia.

出版信息

Plant Physiol. 2001 Apr;125(4):1788-801. doi: 10.1104/pp.125.4.1788.

Abstract

Flowering (inflorescence formation) of the grass Lolium temulentum is strictly regulated, occurring rapidly on exposure to a single long day (LD). During floral induction, L. temulentum differs significantly from dicot species such as Arabidopsis in the expression, at the shoot apex, of two APETALA1 (AP1)-like genes, LtMADS1 and LtMADS2, and of L. temulentum LEAFY (LtLFY). As shown by in situ hybridization, LtMADS1 and LtMADS2 are expressed in the vegetative shoot apical meristem, but expression increases strongly within 30 h of LD floral induction. Later in floral development, LtMADS1 and LtMADS2 are expressed within spikelet and floret meristems and in the glume and lemma primordia. It is interesting that LtLFY is detected quite late (about 12 d after LD induction) within the spikelet meristems, glumes, and lemma primordia. These patterns contrast with Arabidopsis, where LFY and AP1 are consecutively activated early during flower formation. LtMADS2, when expressed in transgenic Arabidopsis plants under the control of the AP1 promoter, could partially complement the organ number defect of the severe ap1-15 mutant allele, confirming a close relationship between LtMADS2 and AP1.

摘要

毒麦的开花(花序形成)受到严格调控,在暴露于单个长日照(LD)时会迅速发生。在花诱导过程中,毒麦在茎尖处两个类APETALA1(AP1)基因LtMADS1和LtMADS2以及毒麦LEAFY(LtLFY)的表达上与拟南芥等双子叶植物有显著差异。原位杂交显示,LtMADS1和LtMADS2在营养茎尖分生组织中表达,但在长日照花诱导30小时内表达强烈增加。在花发育后期,LtMADS1和LtMADS2在小穗和小花分生组织以及颖片和外稃原基中表达。有趣的是,在小穗分生组织、颖片和外稃原基中相当晚(长日照诱导后约12天)才检测到LtLFY。这些模式与拟南芥形成对比,在拟南芥中,LFY和AP1在花形成早期相继被激活。当LtMADS2在AP1启动子控制下在转基因拟南芥植物中表达时,它可以部分弥补严重的ap1 - 15突变等位基因的器官数量缺陷,证实了LtMADS2与AP1之间的密切关系。

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