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Tilletia horrida glycoside hydrolase family 128 protein, designated ThGhd_7, modulates plant immunity by blocking reactive oxygen species production

文献类型： 外文期刊

作者： Shu, Xinyue 1 ; Yin, Desuo 3 ; Liang, Juan 1 ; Xiang, Ting 1 ; Zhang, Chao 1 ; Li, Honglian 1 ; Zheng, Aiping 2 ; Li, Ping 4 ; Wang, Aijun 1 ;

作者机构： 1.Henan Agr Univ, Coll Plant Protect, Engn Res Ctr Plant Hlth Protect Technol Henan Prov, Zhengzhou, Peoples R China

2.Sichuan Agr Univ, Coll Agron, Chengdu, Peoples R China

3.Hubei Acad Agr Sci, Food Crop Res Inst, Wuhan, Peoples R China

4.Sichuan Agr Univ, Rice Res Inst, Chengdu 611130, Peoples R China

5.Henan Agr Univ, Coll Plant Protect, Zhengzhou 450046, Peoples R China

关键词： defence response; effector; reactive oxygen species; rice; Tilletia horrida

期刊名称：PLANT CELL AND ENVIRONMENT （ 影响因子：7.3； 五年影响因子：8.1 ）

ISSN： 0140-7791

年卷期： 2024 年 47 卷 7 期

页码：

收录情况： SCI

摘要： Tilletia horrida is an important soilborne fungal pathogen that causes rice kernel smut worldwide. We found a glycoside hydrolase family 128 protein, designated ThGhd_7, caused cell death in Nicotiana benthamiana leaves. The predicted signal peptide (SP) of ThGhd_7 targets it for secretion. However, loss of the SP did not affect its ability to induce cell death. The 23-201 amino acid sequence of ThGhd_7 was sufficient to trigger cell death in N. benthamiana. ThGhd_7 expression was induced and upregulated during T. horrida infection. ThGhd_7 localised to both the cytoplasm and nucleus of plant cells, and nuclear localisation was required to induce cell death. The ability of ThGhd_7 to trigger cell death in N. benthamiana depends on RAR1 (required for Mla12 resistance), SGT1 (suppressor of G2 allele of Skp1), and BAK1/SERK3 (somatic embryogenesis receptor-like kinase 3). Heterologous overexpression of ThGhd_7 in rice reduced reactive oxygen species (ROS) production and enhanced susceptibility to T. horrida. Further research revealed that ThGhd_7 interacted with and destabilised OsSGT1, which is required for ROS production and is a positive regulator of rice resistance to T. horrida. Taken together, these findings suggest that T. horrida employs ThGhd_7 to disrupt ROS production and thereby promote infection.

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