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| 1 | Interactions between HLH and bHLH Factors Modulate Light-Regulated Plant Development显示文摘Phytochromes (Phy ) 和因素(程序信息文件) 抄写因素组成一个主要发信号的交往 phytochrome 响应红和 far-red 光控制植物开发的模块。当由邻居的 shading 种并且导致称为阴影回避症候群(SAS ) 的房间 elongationa 现象,低 red:far 红的比率被解释。PAR1 和它的最靠近的相当或相同的事物 PAR2 是 SAS 的否定管理者;他们属于缺乏要求的典型的基本的域的 HLH 抄写因素家庭因为 DNA 绑定,和他们被相信通过还有待于被识别的 DNA 有约束力的抄写因素调整基因表达式。这里,我们证明那个轻信号稳定 PAR1 蛋白质, PAR1 与 PIF4 交往并且禁止调停 PIF4 的基因激活。DNA 下拉和染色质 immunoprecipitation (薄片) 试金证明 PAR1 禁止在 vitro 并且在 vivo 有约束力的 PIF4 DNA。转基因的植物 overexpressing PAR1 (PAR1OX ) 在胚轴延伸对赤霉素(GA ) 或高温度感觉迟钝,同样到 pifq 异种。除了 PIF4, PAR1 也与 PRE1, brassinosteroid (BR ) 激活的一个 HLH 抄写因素和 GA 交往。PRE1 的 Overexpression 大部分压制了 PAR1OX 的矮子显型。这些结果显示 PAR1PRE1 和 PAR1PIF4 heterodimers 形成响应光和荷尔蒙调整房间延伸和植物开发的一个复杂 HLH/bHLH 网络。 | Yaqi Hao Eunkyoo Oh GUtsu Choi Zongsuo Liang Zhi-Yong Wang | 2012 | Molecular Plant2012，5，3： | 19 |
| 2 | Light activates the degradation of PIL5 protein to promote seed germination through gibberellin in Arabidopsis 显示文摘 | Eunkyoo O Shinjiro Y Yuji K | 2006 | The Plant Journal2006，47，： | 1 |
| 3 | Light activates the degradation of PIL 5 protein to promote seed germination through gibberellin in Arabidopsis显示文摘 | EUNKYOO O SHINJIRO Y YUJI K | 2006 | The Plant Journal2006，47，： | 1 |
| 4 | Integration of Brassinosteroid Signal Transduction with the Transcription Network for Plant Growth Regulation in Arabidopsis显示文摘 | Yu Sun Xi-Ying Fan Dong-Mei Cao Wenqiang Tang Kun He Jia-Ying Zhu Jun-Xian He Ming-Yi Bai Shengwei Zhu Eunkyoo Oh Sunita Patil Tae-Wuk Kim Hongkai Ji Wing Hong Wong Seung Y. Rhee Zhi-Yong Wang | 2010 | Developmental Cell2010，，5： | 1 |
| 5 | Chemical control of receptor kinase signaling by rapamycin-induced dimerization显示文摘Membrane-localized leucine-rich repeat receptor kinases(LRR-RKs)sense diverse extracellular signals,and coordinate and specify cellular functions in plants.However,functional understanding and identification of the cellular signaling of most LRR-RKs remain a major challenge owing to their genetic redundancy,the lack of ligand information,and subtle phenotypes of LRR-RK overexpression.Here,we report an engineered rapamycin-inducible dimerization(RiD)receptor system that triggers a receptor-specific LRR-RK signaling independent of their cognate ligands or endogenous receptors.Using the RiD-receptors,we demonstrated that the rapamycin-mediated association of chimeric cytosolic kinase domains from the BRI1/BAK1 receptor/co-receptor,but not the BRI1/BRI1 or BAK1/BAK1 homodimer,is sufficient to activate downstream brassinosteroid signaling and physiological responses.Furthermore,we showed that the engineered RiD-FLS2/BAK1 could activate flagellin-22-mediated immune signaling and responses.Using the RiD system,we also identified the potential function of an unkmown orphan receptor in immune signaling and revealed the differential activities of SERK co-receptors of LRR-RKs.Our results indicate that the RiD method can serve as a synthetic biology tool for precise temporal manipulation of LRR-RK signaling and for understanding LRR-RK biology. | Sara Kim Jeonghyang Park Byeong Wook Jeon Geonhee Hwang Na Young Kang Yeim We Won-Young Park Eunkyoo Oh Jungmook Kim | 2021 | Molecular Plant2021，14，8： | 0 |
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