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拟南芥中APETALA3和PISTILLATA对花同源异型基因APETALA1的直接调控

Direct regulation of the floral homeotic APETALA1 gene by APETALA3 and PISTILLATA in Arabidopsis.

作者信息

Sundström Jens F, Nakayama Naomi, Glimelius Kristina, Irish Vivian F

机构信息

Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT 06520-8104, USA.

出版信息

Plant J. 2006 May;46(4):593-600. doi: 10.1111/j.1365-313X.2006.02720.x.

Abstract

The floral homeotic gene APETALA1 (AP1) specifies floral meristem identity and sepal and petal identity in Arabidopsis. Consistent with its multiple roles during floral development, AP1 is initially expressed throughout the floral meristem, and later its expression becomes restricted to sepal and petal primordia. Using chromatin immunoprecipitation, we show that the floral homeotic PISTILLATA (PI) protein, required for petal and stamen development, has the ability to bind directly to the promoter region of AP1. In support of the hypothesis that PI, and its interacting partner APETALA3 (AP3), regulates the transcription of AP1, we show that AP1 transcript levels are elevated in strong ap3-3 mutant plants. Kinetic studies, using transgenic Arabidopsis plants in which both AP3 and PI are under post-translational control, show that AP1 transcript levels are down regulated within 2 h of AP3/PI activation. This implies that the reduction in AP1 transcripts is an early event in the cascade following AP3/PI induction and provides independent support for the hypothesis that AP1 is a direct target of the AP3/PI heterodimer. Together these results suggest a model whereby AP3/PI directly acts, in combination with other factors, to restrict the expression of AP1 during early stages of floral development.

摘要

花同源异型基因APETALA1(AP1)决定了拟南芥花分生组织的特征以及萼片和花瓣的特征。与它在花发育过程中的多种作用相一致,AP1最初在整个花分生组织中表达,随后其表达局限于萼片和花瓣原基。利用染色质免疫沉淀技术,我们发现花瓣和雄蕊发育所必需的花同源异型PISTILLATA(PI)蛋白能够直接结合到AP1的启动子区域。为支持PI及其相互作用伴侣APETALA3(AP3)调节AP1转录的假说,我们发现AP1转录水平在强ap3 - 3突变体植株中升高。利用AP3和PI均处于翻译后调控状态的转基因拟南芥植株进行的动力学研究表明,在AP3/PI激活后2小时内,AP1转录水平下调。这意味着AP1转录本的减少是AP3/PI诱导后级联反应中的早期事件,并为AP1是AP3/PI异二聚体的直接靶标的假说提供了独立支持。这些结果共同表明了一个模型,即AP3/PI与其他因子共同作用,在花发育早期直接限制AP1的表达。

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