烟草TTG2蛋白质对NPR1介导的抗病防卫反应与ARF8影响的生长发育进行交叉调控的机制  

Molecular Mechanisms Underlying the Roles of the TTG2 Protein in Modulating NPR1-Regulated Pathogen Defenses and ARF8-Engaged Development in Tobacco

作　　者：韩冰[1] 朱茜[1] 葛军[1] 徐曼宇 董汉松[1] 

机构地区：[1]南京农业大学植物保护学院,南京210095

出　　处：《植物生理学报》2013年第12期1291-1300,共10页Plant Physiology Journal

基　　金：国家自然科学基金(31171830和31272027)

摘　　要：NPR1蛋白是水杨酸信号和系统获得性抗性的转录调节因子,它的功能受蛋白质降解酶体CUL3-E3的控制。植物的发育主要受生长素信号通路的控制,生长素反应因子(ARF)参与生长素信号转导转录调控。植物转录因子NPR1和ARF8分别在蛋白质降解酶体CUL3-E3与CUL1-E3控制下,调控抗病防卫与生长发育。烟草TTG2促进ARF8从细胞质向细胞核转运及其转录调控作用,因此促进生长发育;相反,TTG2把NPR1扣留在细胞质,阻止它对防卫反应基因的转录调控作用,从而抑制抗病性。TTG2与NPR1或ARF8并不直接互作,说明存在协助因子。The NPR1 （nonexpressor of pathogenesis-related genes 1） protein is a transcription regulator of salicylic acid （SA） signaling and systemic acquired resistance, and the protein functions under the control of the cullin 3-based E3 ligase （CUL3-E3） proteasome in plants. In frequent crosstalk with the resistance, plant development is largely regulated by the auxin signaling pathway, which depends on auxin response factor （ARF） proteins to regulate auxin responses of plants. The transcriptional function of ARFs is repressed when binding to Aux/IAA proteins, and activated by the CUL l-E3 proteasome, which degrades Aux/IAA to release ARFs. The defensive role of NPR1 and the developmental role of ARF8 were oppositely regulated by the TRANSPARENT TESTA GLABRA 2 （TTG2） protein in tobacco. TTG2 suppresses resistance to viral and bacterial pathogens by sequestering NPR1 from the nucleus but promotes the developmental role of ARF8 by facilitating its localization to the nucleus. However, TTG2 does not directly interact with NPR1 or ARF8, suggesting that potential proteins assist TTG2 in modulating the nucleocytoplasmic transports. Starting with identifying the postulated assistant factors, this report aims to elucidate the mechanism of TTG2 modulating the nucleocvtoolasmic traffickin of NPR1 and ARF8 and the following impact on E3 proteasome.

关 键 词：TTG2 交叉调控 抗病防卫 生长发育 信号转导 

分 类 号：S572[农业科学—烟草工业]