CBL-interacting protein kinase 31 regulates rice resistance to blast disease by modulating cellular potassium levels

文献类型： 外文期刊

第一作者： Lin, Qiu Jun

作者： Lin, Qiu Jun;Li, Zhi Min;Wu, Xian Xin;Sun, Qian;Xuan, Yuan Hu;Kumar, Vikranth;Chu, Jin;Dong, Hai

作者机构：

关键词： CBL; CIPK31; Defense; Rice blast; Potassium

期刊名称：BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS （ 影响因子：3.575； 五年影响因子：3.381 ）

ISSN： 0006-291X

年卷期： 2021 年 563 卷

页码：

收录情况： SCI

摘要： Rice blast disease caused by infection with Magnaporthe oryzae, a hemibiotrophic fungal pathogen, significantly reduces the yield production. However, the rice defense mechanism against blast disease remains elusive. To identify the genes involved in the regulation of rice defense to blast disease, dissociation (Ds) transposon tagging mutant lines were analyzed in terms of their response to M. oryzae isolate Guy11. Among them, CBL-interacting protein kinase 31 (CIPK31) mutants were more susceptible than wild-type plants to blast. The CIPK31 transcript was found to be insensitive to Guy11 infection, and the CIPK31-GFP was localized to the cytosol and nucleus. Overexpression of CIPK31 promoted rice defense to blast. Further analysis indicated that CIPK31 interacts with Calcineurin B-like 2 (CBL2) and CBL6 at the plasma membrane, and cbl2 mutants are more susceptible to blast compared with wild-type plants, suggesting that calcium signaling might partially through the CBL2-CIPK31 signaling regulate rice defense. Yeast two-hybrid results showed that AKT1-like (AKT1L), a potential potassium (K+) channel protein, interacted with CIPK31, and the K+ level was significantly lower in the cipk31 mutants than in the wild-type control. In addition, exogenous potassium application increased rice resistance to blast, suggesting that CIPK31 might interact with AKT1L to increase K+ uptake, thereby promoting resistance to blast. Taken together, the results presented here demonstrate that CBL2-CIPK31-AKT1L is a new signaling pathway that regulates rice defense to blast disease. (C) 2021 Elsevier Inc. All rights reserved.

分类号：

  • 相关文献
作者其他论文 更多>>

微信小程序