1. Genome-wide identification of Brassinosteroid insensitive 1-associated receptor kinase 1 genes and expression analysis in response to pathogen infection in cucumber (Cucumis sativus L.)
- Author
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Jianan Han, Shaoyun Dong, Jiantao Guan, Xiaoping Liu, Xingfang Gu, Han Miao, and Shengping Zhang
- Subjects
Cucumis sativus L. ,BAK1 ,Gene family ,Expression pattern ,Pathogen infection ,Botany ,QK1-989 - Abstract
Abstract Background BAK1 (Brassinosteroid insensitive 1-associated receptor kinase 1) plays an important role in disease resistance in plants. However, the function of BAK1 family in cucumber and the decisive genes for disease-resistance remain elusive. Results Here, we identified 27 CsBAK1s in cucumber, and classified them into five subgroups based on phylogenetic analysis and gene structure. CsBAK1s in the same subgroup shared the similar motifs, but different gene structures. Cis-elements analysis revealed that CsBAK1s might respond to various stress and growth regulation. Three segmentally duplicated pairwise genes were identified in cucumber. In addition, Ka/Ks analysis indicated that CsBAK1s were under positive selection during evolution. Tissue expression profile showed that most CsBAK1s in Subgroup II and IV showed constitutive expression, members in other subgroups showed tissue-specific expression. To further explore whether CsBAK1s were involved in the resistance to pathogens, the expression patterns of CsBAK1s to five pathogens (gummy stem blight, powdery mildew, downy mildew, grey mildew, and fusarium wilt) reveled that different CsBAK1s had specific roles in different pathogen infections. The expression of CsBAK1-14 was induced/repressed significantly by five pathogens, CsBAK1-14 might play an important role in disease resistance in cucumber. Conclusions 27 BAK1 genes were identified in cucumber from a full perspective, which have important functions in pathogen infection. Our study provided a theoretical basis to further clarify the function of BAK1s to disease resistance in cucumber.
- Published
- 2024
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