Pathogenicity Variation in Two Genomes of Cercospora Species Causing Gray Leaf Spot in Maize

文献类型： 外文期刊

第一作者： Cheng, Zixiang

作者： Cheng, Zixiang;Duan, Canxing;Xu, Zhennan;Li, Mingshun;Hao, Zhuafang;Li, Xinhai;Weng, Jianfeng;Lv, Xiangling;Yin, Huifei;Zhou, Xiaohang;Li, Fenghai;Zhu, Hanyong;Wang, Jianjun

作者机构： Chinese Acad Agr Sci, Inst Crop Sci, Beijing 100081, Peoples R China;Shenyang Agr Univ, Coll Agron, Shenyang 110161, Liaoning, Peoples R China;Wenshan Acad Agr Sci, Wenshan 663000, Yunnan, Peoples R China;Shanxi Agr Univ, Corn Res Inst, Xinzhou 030600, Shanxi, Peoples R China

关键词： Cercospora zeae-maydis; Cercospora zeina; gray leaf spot; Nanopore sequencing; pathogenicity

期刊名称：MOLECULAR PLANT-MICROBE INTERACTIONS （ 2022影响因子：3.5； 五年影响因子：4.1 ）

ISSN： 0894-0282

年卷期： 2023 年 36 卷 1 期

页码：

收录情况： SCI

摘要： The gray leaf spots caused by Cercospora spp. severely affect the yield and quality of maize. However, the evolutionary relation and pathogenicity variation between species of the Cercospora genus is largely unknown. In this study, we constructed high-quality reference genomes by nanopore sequencing two Cercospora species, namely, C. zeae-maydis and C. zeina, with differing pathogenicity, collected from northeast (Liaoning [LN]) and southeast (Yunnan [YN]) China, respectively. The genome size of C. zeae-maydis-LN is 45.08 Mb, containing 10,839 annotated genes, whereas that of Cercospora zeina-YN is 42.18 Mb, containing 10,867 annotated genes, of which approximately 86.58% are common in the two species. The difference in their genome size is largely attributed to increased long terminal repeat retrotransposons of 3.8 Mb in total length in C. zeae-maydis-LN. There are 41 and 30 carbohydrate-binding gene subfamilies identified in C. zeae-maydis-LN and C. zeina-YN, respectively. A higher number of carbohydrate-binding families found in C. zeae-maydis-LN, and its unique CBM4, CBM37, and CBM66, in particular, may contribute to variation in pathogenicity between the two species, as the carbohydrate-binding genes are known to encode cell wall-degrading enzymes. Moreover, there are 114 and 107 effectors predicted, with 47 and 46 having unique potential pathogenicity in C. zeae-maydis-LN and C. zeina-YN, respectively. Of eight effectors randomly selected for pathogenic testing, five were found to inhibit cell apoptosis induced by Bcl-2-associated X. Taken together, our results provide genomic insights into variation in pathogenicity between C. zeae-maydis and C. zeina.

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