通过分析水杨酸合成关键酶基因ICS1的启动子，鉴别出了具有负调控功能的区段；利用酵母单杂交筛选，鉴别出了转录因子TCP8。TCP8受多种胁迫信号诱导，且可以特异结合ICS1启动子；TCP8单突变体中未发现水杨酸信号的显著改变，但过量表达TCP8可以显著抑制胁迫诱导下ICS1的表达及水杨酸信号，表明TCP8可能通过负调控ICS1的表达参与诱导下的水杨酸平衡调控。此外，过量表达TCP8或抑制TCP8下游基因的表达均显著改变了拟南芥的生长与发育进程，显示其在生长发育过程中可能发挥着重要的作用。本项目拟开展以下研究：1）明确TCP8对ICS1的表达调控作用机制，鉴别功能冗余的TCP蛋白；2）探明TCPs与其它ICS1负调控因子的协同调控机制；3）阐明TCPs通过ICS1/SA的节点调控其它生长发育过程的关系，以便于全面理解ICS1节点/SA信号途径在植物生长发育中的广谱作用机理。

An upstream fragment involved in the negative regulation of the expression of ICS1, a key enzyme in the biochemical pathway of salicylic acid biosynthesis in Arabidopsis, was identified by dissecting its promoter region, and subsequently, a TCP transcription factor, AtTCP8, was isolated by yeast one-hybrid screening and its binding to the promoter of ICS1 confirmed. Although tcp8-1 did not show any obvious phenotype involved in SA signaling, over-expression of AtTCP8 significantly repressed ICS1 expression under various stresses, demonstrating that AtTCP8 was a direct negative regulator of ICS1 expression in SA signaling. Besides, either over-expression of AtTCP8 or repression of its downstream gene expression produced significant/dramatic impacts on plant growth and development. This project is designed to pursue further explorations in following aspects: 1) to thoroughly explore the regulation of ICS1 expression by AtTCP8, and to identify redundant TCP protein(s) with similar function; 2) to explore the coordinated regulatory mechanism of different negative regulators involved in the regulation of ICS1; 3) to reveal the mechanisms of plant growth and development associated with ICS1 and/or SA signaling regulated by AtTCP8 and related TCP transcription factor(s).