LEAFY COTYLEDON1-CASEIN KINASE I-TCP15-PHYTOCHROME INTERACTING FACTOR4 Network Regulates Somatic Embryogenesis by Regulating Auxin Homeostasis
LEAFY COTYLEDON1-CASEIN KINASE I-TCP15-PHYTOCHROME INTERACTING FACTOR4 Network Regulates Somatic Embryogenesis by Regulating Auxin Homeostasis
复制标题
叶状子叶1-酪蛋白激酶I-TCP15-植物色素相互作用因子4网络通过调节生长素稳态来调节体细胞胚胎发生
DOI：
10.1104/pp.15.01480
复制
发表时间：
2015-12-01
期刊：
影响因子：
7.4
通讯作者：
Zhang, Xianlong
中科院分区：
文献类型：
--
作者：
Min, Ling;Hu, Qin;Zhang, Xianlong
体细胞胚胎发生是植物物种繁殖的有效工具，也是研究胚胎发育调控网络的有效模型。然而，在SE过程中，从非胚性愈伤组织向体细胞胚胎转变的调控网络仍然知之甚少。在这里，我们描述了一个陆地棉花（棉）酪蛋白激酶I基因，GhCKI，这是一个独特的关键调控因子，强烈影响SE。由于GhCKI的过表达阻碍了非胚性愈伤组织向体细胞胚的转变，从而阻止了胚状体的形成和植株的再生。相反，植物GhCKI缺陷促进了SE的发生。为了更好地理解GhCKI调控SE的机制，我们分析了GhCKI调控网络。一个直接上游负调节蛋白棉花叶型COTYLEDON1被鉴定为靶向GhCKI启动子中的顺式元件CTTTTC。此外，GhCKI与棉花cincinnati -like TEOSINTE BRANCHED1-CYCLOIDEA-PCF转录因子15相互作用并磷酸化，通过协调调节棉花光光色素相互作用因子4的表达，最终破坏生长素的稳态，导致过表达GhCKI的体细胞细胞增殖增加和体胚形成流产。我们的研究结果表明，一个复杂的SE过程是由GhCKI通过一个复杂的调控网络负调控的。
Somatic embryogenesis (SE) is an efficient tool for the propagation of plant species and also, a useful model for studying the regulatory networks in embryo development. However, the regulatory networks underlying the transition from nonembryogenic callus to somatic embryos during SE remain poorly understood. Here, we describe an upland cotton (Gossypium hirsutum) CASEIN KINASE I gene, GhCKI, which is a unique key regulatory factor that strongly affects SE. Overexpressing GhCKI halted the formation of embryoids and plant regeneration because of a block in the transition from nonembryogenic callus to somatic embryos. In contrast, defective GhCKI in plants facilitated SE. To better understand the mechanism by which GhCKI regulates SE, the regulatory network was analyzed. A direct upstream negative regulator protein, cotton LEAFY COTYLEDON1, was identified to be targeted to a cis-element, CTTTTC, in the promoter of GhCKI. Moreover, GhCKI interacted with and phosphorylated cotton CINCINNATA-like TEOSINTE BRANCHED1-CYCLOIDEA-PCF transcription factor15 by coordinately regulating the expression of cotton PHYTOCHROME INTERACTING FACTOR4, finally disrupting auxin homeostasis, which led to increased cell proliferation and aborted somatic embryo formation in GhCKI-overexpressing somatic cells. Our results show a complex process of SE that is negatively regulated by GhCKI through a complex regulatory network.