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CmFTL3 缺失一个残基会导致成花素无法开花。

The loss of a single residue from CmFTL3 leads to the failure of florigen to flower.

机构信息

College of Horticulture, Nanjing Agricultural University, Key Laboratory of Landscaping, Ministry of Agriculture, Nanjing 210095, China.

College of Horticulture, Nanjing Agricultural University, Key Laboratory of Landscaping, Ministry of Agriculture, Nanjing 210095, China.

出版信息

Plant Sci. 2018 Nov;276:99-104. doi: 10.1016/j.plantsci.2018.08.005. Epub 2018 Aug 14.

DOI:10.1016/j.plantsci.2018.08.005
PMID:30348332
Abstract

The product of CmFTL, a gene represented by multiple transcripts, is an important determinant of floral development in chrysanthemum. Here, a new transcript CmFTL3ps4 which contains three different amino acid residues compared to CmFTL3 was characterized. When driven by the Arabidopsis thaliana FT promoter, CmFTL3ps4 expression did not rescue the late flowering phenotype of the A. thaliana ft-10 mutant. When the variant sequences CmFTL3, CmFTL3 and CmFTL3 were heterologously expressed in A. thaliana, both CmFTL3 and CmFTL3 were shown to accelerate flowering, although to a different extent. There was no significant difference in the number of leaves which had formed before the flowering of either the CmFTL3 or the CmFTL3ps4 transgenic lines. Neither the transgenic expression of CmFTL3ps4 or CmFTL3 was able to rescue the ft-10 mutant phenotype. A bimolecular fluorescence complementation assay confirmed that CmFTL3 did not interact with CmFDL1, a homolog of the bZIP transcription factor FD. The conclusion was that a novel residue change affected FT activity through its disruption of the interaction with CmFDL1.

摘要

CmFTL 是一个由多个转录本所代表的基因,其产物是菊花花发育的一个重要决定因素。在这里,我们对一种新的转录本 CmFTL3ps4 进行了研究,它与 CmFTL3 相比有三个不同的氨基酸残基。当由拟南芥 FT 启动子驱动时,CmFTL3ps4 的表达并不能挽救拟南芥 ft-10 突变体的晚花表型。当变体序列 CmFTL3、CmFTL3 和 CmFTL3 在拟南芥中异源表达时,发现 CmFTL3 和 CmFTL3 都能加速开花,尽管程度不同。在开花前,CmFTL3 或 CmFTL3ps4 转基因系的叶片数量没有明显差异。CmFTL3ps4 或 CmFTL3 的转基因表达均不能挽救 ft-10 突变体的表型。双分子荧光互补测定证实 CmFTL3 与 bZIP 转录因子 FD 的同源物 CmFDL1 不相互作用。结论是,一个新的残基变化通过破坏与 CmFDL1 的相互作用影响了 FT 的活性。

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