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通过在阿拉比多普西斯中通过组织素乙化调节开花时间

Yuehui He¹, Scott D Michaels, Richard M Amasino

¹Department of Biochemistry, University of Wisconsin, Madison, WI 53706, USA.

Science (New York, N.Y.)

|November 1, 2003

概括

阿拉比多普西斯的自主途径使用花D (FLD) 通过去乙化组织素来促进开花,这抑制了花C (FLC) 表达. 这种表观遗传调节对于过渡到生殖发育至关重要.

科学领域:

植物分子生物学植物分子生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
阿拉比多普西斯塔利亚纳研究研究

背景情况:

在植物中,向开花的过渡是一个由多个遗传通路调节的关键发育过程.
阿拉比多普西斯的自主通路促进了不依赖于光和温度等环境线索的开花.
开花地点C (FLC) 是开花的关键抑制剂,其抑制是自主途径的目标.

研究的目的:

为了研究在阿拉比多普西斯的自主花促进途径中,花LOCUS D (FLD) 基因功能的分子机制.
为了确定FLD在调节FLOWERING LOCUS C (FLC) 基因表达中的作用.
为了阐明 histone deacetylation 对花过渡控制的贡献.

主要方法:

在Arabidopsis thaliana中对FLD突变的遗传分析.
染色体免疫沉以评估FLC位点上的基因素乙化水平.
基因表达分析以量化FLC转录水平.

主要成果:

在FLD的突变导致与FLC基因相关的组织蛋白的过乙化.
FLD病变导致FLC的表达增加,导致严重延迟的开花.
FLD编码了组织素脱乙酶复合物的植物同源,将表观遗传修饰与花促进联系起来.

结论:

通过FLD,自主途径通过在FLC位点调解素脱乙烯化来调节开花.
通过FLD去乙化组合体是抑制FLC和促进花过渡的重要机制.
自主途径采用多种策略来抑制FLC,因为并非所有突变物都表现出FLC过乙化.

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