Fobert Pierre R, Després Charles
National Research Council Canada, Plant Biotechnology Institute, 110 Gymnasium Place, Saskatoon, Saskatchewan, S7N 0W9, Canada.
Curr Opin Plant Biol. 2005 Aug;8(4):378-82. doi: 10.1016/j.pbi.2005.05.003.
Changes in gene expression during systemic acquired resistance (SAR) require the phenolic signaling molecule salicylic acid (SA) and are modulated by the interaction between the NON EXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1) protein and members of the TGA family of transcription factors. In the past two years, the activities of NPR1 and of the TGA factors TGA1 and TGA4 have been shown to be modulated by SA-induced oxidoreduction (redox) modifications of key cysteine residues. Reduction of two conserved cysteines in NPR1 leads to its monomerization and nuclear localization, which is required for the activation of PATHOGENESIS-RELATED(PR) genes. Reduction of conserved cysteines in TGA1 and TGA4 enables their interaction with NPR1, which acts as a redox-sensitive cofactor in stimulating TGA1 DNA-binding activity. The identity of the redox mediators that are involved in regulating NPR1 and TGA factors is unknown. However, a novel thioredoxin interacts with the disease resistance protein Cf-9 and modulates Cf-9-dependent signaling. These results begin to provide a mechanistic understanding of how SAR is regulated by redox conditions.
系统获得性抗性（SAR）过程中的基因表达变化需要酚类信号分子水杨酸（SA），并受病程相关基因非表达子1（NPR1）蛋白与TGA转录因子家族成员之间的相互作用调控。在过去两年中，已证明NPR1以及TGA因子TGA1和TGA4的活性受SA诱导的关键半胱氨酸残基氧化还原修饰的调节。NPR1中两个保守半胱氨酸的还原导致其单体化和核定位，这是激活病程相关（PR）基因所必需的。TGA1和TGA4中保守半胱氨酸的还原使其能够与NPR1相互作用，NPR1作为氧化还原敏感的辅因子刺激TGA1的DNA结合活性。参与调节NPR1和TGA因子的氧化还原介质的身份尚不清楚。然而，一种新型硫氧还蛋白与抗病蛋白Cf-9相互作用并调节Cf-9依赖性信号传导。这些结果开始为氧化还原条件如何调节SAR提供了机制上的理解。
