Overexpression of Calcineurin B-like Interacting Protein Kinase 31 Promotes Lodging and Sheath Blight Resistance in Rice

Author:

Chen Jingsheng1,Wang Siting2,Jiang Shiqi1,Gan Tian1,Luo Xin1ORCID,Shi Rujie1,Xuan Yuanhu34,Xiao Guosheng1ORCID,Chen Huan5ORCID

Affiliation:

1. College of Biology and Food Engineering, Chongqing Three Gorges University, Wanzhou 404100, China

2. College of Plant Protection, Shenyang Agricultural University, Shenyang 110866, China

3. State Key Laboratory of Elemento-Organic Chemistry, Nankai University, Tianjin 300071, China

4. Department of Plant Protection, National Pesticide Engineering Research Center (Tianjin), Nankai University, Tianjin 300071, China

5. Key Laboratory of Saline-Alkali Vegetation Ecology Restoration, Ministry of Education, Northeast Forestry University, Harbin 150040, China

Abstract

A breakthrough “Green Revolution” in rice enhanced lodging resistance by using gibberellin-deficient semi-dwarf varieties. However, the gibberellic acid (GA) signaling regulation on rice disease resistance remains unclear. The resistance test showed that a positive GA signaling regulator DWARF1 mutant d1 was more susceptible while a negative GA signaling regulator Slender rice 1 (SLR1) mutant was less susceptible to sheath blight (ShB), one of the major rice diseases, suggesting that GA signaling positively regulates ShB resistance. To isolate the regulator, which simultaneously regulates rice lodging and ShB resistance, SLR1 interactors were isolated. Yeast two-hybrid (Y2H), bimolecular fluorescence complementation (BiFC), and Co-IP assay results indicate that SLR1 interacts with Calcineurin B-like-interacting protein kinase 31 (CIPK31). cipk31 mutants exhibited normal plant height, but CIPK31 OXs showed semi-dwarfism. In addition, the SLR1 level was much higher in CIPK31 OXs than in the wild-type, suggesting that CIPK31 OX might accumulate SLR1 to inhibit GA signaling and thus regulate its semi-dwarfism. Recently, we demonstrated that CIPK31 interacts and inhibits Catalase C (CatC) to accumulate ROS, which promotes rice disease resistance. Interestingly, CIPK31 interacts with Vascular Plant One Zinc Finger 2 (VOZ2) in the nucleus, and expression of CIPK31 accumulated VOZ2. Inoculation of Rhizoctonia solani AG1-IA revealed that the voz2 mutant was more susceptible to ShB. Thus, these data prove that CIPK31 promotes lodging and ShB resistance by regulating GA signaling and VOZ2 in rice. This study provides a valuable reference for rice ShB-resistant breeding.

Funder

Project of Chongqing Science and Technology Commission

Nature Science Foundation of China

Project of Chongqing Three Gorges University High-level Talent Introduction

Project of Wanzhou Science and Technology Bureau

Publisher

MDPI AG

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