Yang Tao, Song Linlin, Hu Jinxian, Qiao Luao, Yu Qing, Wang Zonghua, Chen Xiaofeng, Lu Guo-Dong
State Key Laboratory of Ecological Pest Control for Fujian and Taiwan Crops, College of Plant Protection, Fujian Agriculture and Forestry University, Fuzhou, 35002, China.
Fujian Universities Engineering Research Center of Marine Biology and Drugs, Fuzhou Institute of Oceanography, College of Geography and Oceanography, Minjiang University, Fuzhou, 350108, China.
Rice (N Y). 2024 Feb 13;17(1):14. doi: 10.1186/s12284-024-00693-0.
Rice blast, caused by the fungal pathogen Magnaporthe oryzae, is one of the most devastating diseases for rice crops, significantly affecting crop yield and quality. During the infection process, M. oryzae secretes effector proteins that help in hijacking the host's immune responses to establish infection. However, little is known about the interaction between the effector protein AvrPik-D and the host protein Pikh, and how AvrPik-D increases disease severity to promote infection. In this study, we show that the M. oryzae effector AvrPik-D interacts with the zinc finger-type transcription factor WG7 in the nucleus and promotes its transcriptional activity. Genetic removal (knockout) of the gene WG7 in transgenic rice enhances resistance to M. oryzae and also results in an increased burst of reactive oxygen species after treatments with chitin. In addition, the hormone level of SA and JA, is increased and decreased respectively in WG7 KO plants, indicating that WG7 may negatively mediate resistance through salicylic acid pathway. Conversely, WG7 overexpression lines reduce resistance to M. oryzae. However, WG7 is not required for the Pikh-mediated resistance against rice blast. In conclusion, our results revealed that the M. oryzae effector AvrPik-D targets and promotes transcriptional activity of WG7 to suppress rice innate immunity to facilitate infection.
稻瘟病由真菌病原体稻瘟病菌(Magnaporthe oryzae)引起,是对水稻作物最具毁灭性的病害之一,严重影响作物产量和品质。在感染过程中,稻瘟病菌分泌效应蛋白,这些蛋白有助于劫持宿主的免疫反应以建立感染。然而,关于效应蛋白AvrPik - D与宿主蛋白Pikh之间的相互作用,以及AvrPik - D如何增加病害严重程度以促进感染,人们了解甚少。在本研究中,我们发现稻瘟病菌效应蛋白AvrPik - D在细胞核中与锌指型转录因子WG7相互作用,并促进其转录活性。转基因水稻中基因WG7的遗传去除(敲除)增强了对稻瘟病菌的抗性,并且在用几丁质处理后还导致活性氧爆发增加。此外,SA和JA的激素水平在WG7基因敲除植株中分别升高和降低,这表明WG7可能通过水杨酸途径负向介导抗性。相反,WG7过表达系降低了对稻瘟病菌的抗性。然而,Pikh介导的抗稻瘟病抗性并不需要WG7。总之,我们的结果表明,稻瘟病菌效应蛋白AvrPik - D靶向并促进WG7的转录活性,以抑制水稻的先天免疫从而促进感染。