中文摘要：

TGA基因家族是b ZIP转录因子家族中十分重要的一组,其能够与靶基因启动子上的as-1区域相结合,激活或抑制下游靶标基因的转录,从而调控植株抗性或花器官发育。自烟草中首个TGA基因被鉴定以来,从拟南芥、水稻和苹果等多个物种中均有该家族基因被分离和鉴定出来。拟南芥基因组中共有10个TGA转录因子,依据其序列相似性可将其分为5组（Ⅰ组包含TGA1与TGA4;TGA2、TGA5与TGA6组成第Ⅱ组;TGA3与TGA7组成第Ⅲ组;TGA9和TGA10构成第Ⅳ组;PAN为第Ⅴ组）。其中Ⅰ、Ⅱ与Ⅲ组成员广泛参与植株的抗病反应。酵母双杂交和pull-down等结果显示,TGA1—TGA7均可与水杨酸信号途径关键调节因子NPR1相互作用。EMSA结果表明,这种相互作用能够促进TGA对下游PR1启动子的结合并上调其表达,提高植株抗病性。但这3组基因在植物基础抗性与系统获得抗性中的作用有所不同：tga3突变体对病菌的基础抗性存在缺陷,但植株诱导抗性却并不受影响;TGA1与TGA4对基础抗性和系统抗性均有一定影响;TGA2、TGA5与TGA6之间存在功能冗余,仅tga2/5/6三突变体才表现出与npr1突变体类似的系统获得性抗性缺乏的表型。酵母双杂交筛选发现：Ⅱ组TGA能够与谷氧还蛋白GRX480相互作用并介导SA对JA途径标记基因的抑制作用,同时,该组蛋白还能够与GRAS家族蛋白SCL14相互作用,增强下游CYP81D11与GSTU7等解毒相关基因的表达,以一种不依赖于NPR1的信号途径提高植物对外源化学物质毒害的耐性。此外,tga1/4双突变体与nrt2.1/2.2双突变体的初生根和侧生根生长在低氮条件下较野生型显著下降,Ch IP和酵母单杂交结果显示,TGA1能够与硝酸盐转运蛋白基因NRT2.1及NRT2.2的启动子相互结合,通过调节这两个基因的表达来调节植物的氮响应。而TGA3在镉长距离运输中发挥重要作用。Ⅳ与Ⅴ组成员在调控花器官发育中具有重要作用。tga9/10表现?

英文摘要：

TGA family is an important group of bZIP transcription factors in plant, which regulates the downstream target genes by binding to the as-1 cis-elements in the promoter region and subsequently activating or inhibiting their expression, finally regulating the resistance or development of floral organ. The first TGA gene was identified in tobacco. Subsequently, TGA members were widely characterized in arabidopsis, rice and apple. In arabidopsis, they constitute a multigene family comprising 10 members based on genome sequence analyses. The members of TGA family can be divided into five subgroups （ I ： TGA1 and TGA4; II： TGA2, TGA5 and TGA6; III： TGA3 and TGA7; IV： TGA9 and TGA10; V： PAN） according to their sequence similarity. The members of I, II and III subgroups are mainly involved in disease resistance. Yeast two-hybrid and pull-down results showed that all members of subgroup I, II, and III could interact with NPR1 protein which is the key positive regulator in SA signaling pathway. EMSA results indicated that the interaction between TGA and NPR1 could enhance the expression of pathogenesis-related （PR） genes and disease resistance. However, their roles were different in basal and systemic acquired resistance （SAR）： tga3 mutants showed a defect in basal resistance, whereas the induced resistance was unaffected. TGA1 and TGA4 were involved in regulation of basal resistance and SAR. The tga2/5/6 triple mutants but not tga6 or tga2/5 double mutants were defective in SAR, a phenotype similar to that of the nprl mutants, indicating functional redundancy among TGA2, TGA5 and TGA6. Yeast two-hybrid screen revealed that TGA transcription factors of subgroup II could interact with glutaredoxin GRX480 to mediate the repression of the marker genes of JA signaling by SA, and they also could interact with GRAS protein SCL14 to increase the expression of CYP81D11 and GSTU7 in an NPRl-independent manner and enhance the tolerance to xenobiotics. In addition, the primary and lateral root growth was affe