Direct regulation of the floral homeotic APETALA1 gene by APETALA3 and PISTILLATA in Arabidopsis.
Direct regulation of the floral homeotic APETALA1 gene by APETALA3 and PISTILLATA in Arabidopsis.
复制标题
DOI：
10.1111/j.1365-313x.2006.02720.x
复制
发表时间：
2006-05
期刊：
影响因子：
--
通讯作者：
J. Sundström;N. Nakayama;K. Glimelius;V. Irish
中科院分区：
文献类型：
--
作者：
J. Sundström;N. Nakayama;K. Glimelius;V. Irish
花同源异型基因APETALA 1（AP 1）在拟南芥中指定花分生组织身份以及萼片和花瓣身份。与其在花发育过程中的多重作用相一致，AP 1最初在整个花分生组织中表达，后来其表达仅限于萼片和花瓣原基。使用染色质免疫沉淀，我们表明，花同源异型PISTILLATA（PI）蛋白，花瓣和雄蕊发育所需的，有能力直接结合到启动子区的AP 1。为了支持PI及其相互作用伙伴APETALA 3（AP 3）调节AP 1转录的假设，我们表明AP 1转录水平在强ap 3 -3突变体植物中升高。动力学研究，使用转基因拟南芥植物，其中AP 3和PI都在翻译后控制下，表明AP 1转录水平下调2小时内的AP 3/PI激活。这意味着AP 1转录物的减少是AP 3/PI诱导后级联反应的早期事件，并为AP 1是AP 3/PI异二聚体的直接靶点的假设提供了独立的支持。总之，这些结果表明一个模型，AP 3/PI直接作用，与其他因素相结合，以限制在花发育的早期阶段的AP 1的表达。
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.