Comparative transcriptome analysis of Tilletia horrida infection in resistant and susceptible rice (Oryza sativa L.) male sterile lines reveals potential candidate genes and resistance mechanisms
文献类型： 外文期刊
作者： Wang, Aijun 1 ; Zha, Zhongping 4 ; Yin, Desuo 4 ; Shu, Xinyue 1 ; Ma, Li 1 ; Wang, Linxia 2 ; Li, Ping 2 ; Zheng, Aiping 1 ;
作者机构： 1.State Key Lab Crop Gene Explorat & Utilizat South, Chengdu, Sichuan, Peoples R China
2.Sichuan Agr Univ, Rice Res Inst, Chengdu, Peoples R China
3.Sichuan Agr Univ, Key Lab Sichuan Crop Major Dis, Chengdu, Peoples R China
4.Hubei Acad Agr Sci, Food Crop Res Inst, Wuhan, Hubei, Peoples R China
5.Hubei Key Lab Crop Dis Insect Pest & Weeds Contro, Wuhan, Hubei, Peoples R China
关键词： Tilletia horrida; Transcriptional analysis; Peroxidase activity; Flavonoid biosynthesis; Plant-pathogen interaction
期刊名称：GENOMICS （ 影响因子：5.736； 五年影响因子：4.939 ）
ISSN： 0888-7543
年卷期： 2020 年 112 卷 6 期
页码：
收录情况： SCI
摘要： Rice kernel smut (RKS), caused by the basidiomycete fungus Tilletia horrida, is one of the most devastating diseases affecting the production of male sterile lines of rice (Oryza sativa) worldwide. However, the molecular mechanisms of resistance to T. horrida have not yet been explored. In the present study, RNA sequencing analysis of rice male sterile lines, that are resistant and susceptible to RKS (Jiangcheng 3A and 9311A, respectively) was conducted after T. horrida infection. Transcriptomic analysis showed that a greater number of differentially expressed gene (DEGs) was observed in Jiangcheng 3A compared with 9311A after T. horrida inoculation. Furthermore, 4, 425 DEGs were uniquely detected in Jiangcheng 3A, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of these DEGs revealed that oxidoreductase activity, peroxidase activity, cutin, suberine and wax biosynthesis, and flavonoid biosynthesis were key pathways for T. horrida resistance. In summary and based on transcriptome analysis, we suggest a preliminary regulatory mechanism for Jiangcheng 3A cultivar resistance response to T. horrida inoculation.
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