Isolation of the brassinosteroid receptor genes and recharacterization of dwarf plants by silencing of SlBRI1 in tomato
文献类型: 外文期刊
作者: Zhu, Zhiguo 1 ; Liang, Honglian 1 ; Chen, Guoping 1 ; Tang, Boyan 1 ; Tian, Shibing 2 ; Hu, Zongli 1 ;
作者机构: 1.Chongqing Univ, Bioengn Coll, Minist Educ, Key Lab Biorheol Sci & Technol, Chongqing 400044, Peoples R China
2.Chongqing Acad Agr Sci, Inst Vegetable Res, Chongqing 401329, Peoples R China
关键词: Brassinosteroid receptor; SlBRI1; SlBRI1-like gene; Tomato; Dwarf; Style length
期刊名称:PLANT GROWTH REGULATION ( 影响因子:3.5; 五年影响因子:3.4 )
ISSN: 0167-6903
年卷期: 2019 年 89 卷 1 期
页码:
收录情况: SCI
摘要: Brassinosteroid (BR) is a kind of steroid hormone that is essential for the regulation of multiple processes of plant growth and development, including cell division and elongation, as well as plant resistance to diseases. The BR receptor BRASSINOSTEROID INSENSITIVE1 (BRI1), a multidomain transmembrane receptor-like kinase, roles in BR recognition and signaling. In this study, two putative tomato BR receptor genes were identified, SlBRI1-like 1 (SlBRL1) and SlBRI1-like 2 (SlBRL2). Together with the known receptor gene SlBRI1/CURL3, these three BR receptors had conserved sequence and conformation for their function in BR recognition and kinase activation. Among them, the SlBRI1 was highly expressed in multiple tissues while SlBRLs had a more abundant transcription in the stem, suggesting that they may have a diverse role in tomato growth and development. Corresponding to the expression specificity of SlBRI1, the SlBRI1-RNAi plants exhibited the typical phenotype of reduced plant height, curly dark green leaves and shortened internodes. Meanwhile, the down-regulation of SlBRI1 gave the flower a shorter style than that of wild-type possibly via a SlSTYLE2.1-independent pathway. Additionally, the elevated expression of BR biosynthesis genes SlCPD, SlDWF, SlDET2 and repressed expression of BR inactivation gene SlCYP734A7 revealed the critical role of SlBRI1 in BR pathway-mediated plant architecture and the feedback regulation.
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