Many plant-encoded E3 ligases are known to be involved in plant defense. Here, we report a novel role of E3 ligase SALT- AND DROUGHT-INDUCED RING FINGER1 (SDIR1) in plant immunity. Even though SDIR1 is reasonably well-characterized, its role in biotic stress response is not known. The silencing of SDIR1 in Nicotiana benthamiana reduced the multiplication of the virulent bacterial pathogen Pseudomonas syringae pv. tabaci. The Arabidopsis sdir1 mutant is resistant to virulent pathogens, whereas SDIR1 overexpression lines are susceptible to both host and nonhost hemibiotrophic bacterial pathogens. However, sdir1 mutant and SDIR1 overexpression lines showed hypersusceptibility and resistance, respectively, against the necrotrophic pathogen Erwinia carotovora. The mutant of SDIR1 target protein, i.e., SDIR-interacting protein 1 (SDIR1P1), also showed resistance to host and nonhost pathogens. In SDIR1 overexpression plants, transcripts of NAC transcription factors were less accumulated and the levels of jasmonic acid (JA) and abscisic acid were increased. In the sdir1 mutant, JA signaling genes JAZ7 and JAZ8 were downregulated. These data suggest that SDIR1 is a susceptibility factor and its activation or overexpression enhances disease caused by P. syringae pv. tomato DC3000 in Arabidopsis. Our results show a novel role of SDIR1 in modulating plant defense gene expression and plant immunity.

Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

已知许多植物编码的 E3 连接酶参与植物防御。在这里，我们报告了 E3 连接酶盐和干旱诱导的环指 1 (SDIR1) 在植物免疫中的新作用。尽管 SDIR1 的特征相当明确，但其在生物应激反应中的作用尚不清楚。本塞姆氏烟草中SDIR1的沉默减少了剧毒细菌病原体丁香假单胞菌的增殖。烟粉虱。拟南芥 sdir1突变体对强毒病原体具有抗性，而SDIR1过表达系对宿主和非宿主半生物营养细菌病原体均敏感。然而， sdir1突变体和SDIR1过表达系分别对坏死性病原体胡萝卜软腐欧文氏菌表现出高度敏感性和抗性。 SDIR1靶蛋白的突变体，即SDIR相互作用蛋白1（SDIR1P1），也表现出对宿主和非宿主病原体的抗性。在SDIR1过表达植物中， NAC转录因子的转录物积累较少，茉莉酸（JA）和脱落酸的水平增加。在sdir1突变体中，JA 信号基因JAZ7和JAZ8下调。这些数据表明SDIR1是一种易感因子，其激活或过度表达会增强丁香假单胞菌引起的疾病。拟南芥中的番茄DC3000。我们的结果表明 SDIR1 在调节植物防御基因表达和植物免疫方面具有新作用。

版权所有 © 2021 作者。这是一篇根据 CC BY-NC-ND 4.0 国际许可证分发的开放获取文章。