The thioredoxin GbNRX1 plays a crucial role in homeostasis of apoplastic reactive oxygen species in response to Verticillium dahliae infection in cotton----中国科学院微生物研究所

科研成果

论文题目:	The thioredoxin GbNRX1 plays a crucial role in homeostasis of apoplastic reactive oxygen species in response to Verticillium dahliae infection in cotton
作者:	Li Yuan-Bao, Han Li-Bo, Wang Hai-Yun, Zhang Jie, Sun Shu-Tao, Feng De-Qin, Yang Chun-Lin, Sun Yong-Duo, Zhong Nai-Qin, and Xia Gui-Xian*.
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刊物名称:	Plant Physiol
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年份:	2016
影响因子:	8.03
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摘要:	Examining the proteins that plants secrete into the apoplast in response to pathogen attack provides crucial information for understanding the molecular mechanisms underlying plant innate immunity. In this study, we analyzed the changes in the root apoplast secretome of the Verticillium wilt-resistant island cotton cv. Hai 7124 (G. barbadense) upon infection with Verticillium dahliae. Two-Dimensional Differential Gel Electrophoresis (2D-DIGE) and mass spectrometry (MALDI-TOF/TOF) analysis identified 68 significantly altered spots, corresponding to 49 different proteins. Gene ontology annotation indicated that most of these proteins function in reactive oxygen species (ROS) metabolism and defense response. Of the ROS-related proteins identified, we further characterized a thioredoxin, GbNRX1, which increased in abundance in response to V. dahliae challenge, finding that GbNRX1 functions in apoplastic ROS scavenging after the ROS burst that occurs upon recognition of V. dahliae. Silencing of GbNRX1 resulted in defective dissipation of apoplastic ROS, which led to higher ROS accumulation in protoplasts. As a result, the GbNRX1-silenced plants showed reduced wilt resistance, indicating that the initial defense response in the root apoplast requires the antioxidant activity of GbNRX1. Together, our results demonstrate that apoplastic ROS generation and scavenging occur in tandem in response to pathogen attack; also, the rapid balancing of redox to maintain homeostasis after the ROS burst, which involves GbNRX1, is critical for the apoplastic immune response.