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MEDIATOR SUBUNIT 16 negatively regulates rice immunity by modulating PATHOGENESIS RELATED 3 activity

文献类型: 外文期刊

作者: Zhang, Peng 1 ; Ma, Xiaoding 3 ; Liu, Lina 1 ; Mao, Chanjuan 1 ; Hu, Yongkang 1 ; Yan, Bingxiao 4 ; Guo, Jia 5 ; Liu, Xinyu 6 ; Shi, Jinxia 1 ; Lee, Gang-Seob 7 ; Pan, Xiaowu 8 ; Deng, Yiwen 1 ; Zhang, Zhengguang 1 ; Kang, Zhensheng 5 ; Qiao, Yongli 1 ;

作者机构: 1.Shanghai Normal Univ, Coll Life Sci, Shanghai Key Lab Plant Mol Sci, Shanghai 200234, Peoples R China

2.Yangtze Univ, Coll Agr, Jingzhou 434025, Peoples R China

3.Chinese Acad Agr Sci, Inst Crop Sci, Natl Key Facil Crop Gene Resources & Genet Improve, Beijing 100081, Peoples R China

4.Chinese Acad Sci, Shanghai Inst Plant Physiol & Ecol, CAS Ctr Excellence Mol Plant Sci, Natl Key Lab Plant Mol Genet, Shanghai 200032, Peoples R China

5.Northwest A&F Univ, Coll Plant Protect, State Key Lab Crop Stress Biol Arid Areas, Yangling 712100, Peoples R China

6.Nanjing Agr Univ, Coll Plant Protect, Dept Plant Pathol, Nanjing 210095, Peoples R China

7.Natl Inst Agr Sci, JeonJu 54874, South Korea

8.Hunan Acad Agr Sci, Hunan Rice Res Inst, Changsha 410125, Peoples R China

期刊名称:PLANT PHYSIOLOGY ( 影响因子:7.4; 五年影响因子:8.7 )

ISSN: 0032-0889

年卷期: 2023 年 192 卷 2 期

页码:

收录情况: SCI

摘要: Lesion mimic mutants (LMMs) are valuable genetic resources for unraveling plant defense responses including programmed cell death. Here, we identified a rice (Oryza sativa) LMM, spotted leaf 38 (spl38), and demonstrated that spl38 is essential for the formation of hypersensitive response-like lesions and innate immunity. Map-based cloning revealed that SPL38 encodes MEDIATOR SUBUNIT 16 (OsMED16). The spl38 mutant showed enhanced resistance to rice pathogens Magnaporthe oryzae and Xanthomonas oryzae pv. oryzae (Xoo) and exhibited delayed flowering, while OsMED16-overexpressing plants showed increased rice susceptibility to M. oryzae. The OsMED16-edited rice lines were phenotypically similar to the spl38 mutant but were extremely weak, exhibited growth retardation, and eventually died. The C-terminus of OsMED16 showed interaction with the positive immune regulator PATHOGENESIS RELATED 3 (OsPR3), resulting in the competitive repression of its chitinase and chitin-binding activities. Furthermore, the ospr3 osmed16 double mutants did not exhibit the lesion mimic phenotype of the spl38 mutant. Strikingly, OsMED16 exhibited an opposite function in plant defense relative to that of Arabidopsis (Arabidopsis thaliana) AtMED16, most likely because of 2 amino acid substitutions between the monocot and dicot MED16s tested. Collectively, our findings suggest that OsMED16 negatively regulates cell death and immunity in rice, probably via the OsPR3-mediated chitin signaling pathway. OsMED16 negatively regulates cell death and immunity in rice, probably via the OsPR3-mediated chitin signaling pathway

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