Coumarin Promotes Hypocotyl Elongation in Light-grown Arabidopsis thaliana Seedlings by Enhancing Brassinosteroid Signalling in an Auxin-Dependent Manner

被引:0
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作者
Van Praet, Stan [1 ,2 ,3 ]
Rizza, Annalisa [4 ]
Tang, Bijun [4 ]
Xie, Congwei [1 ,2 ]
Jones, Alexander [4 ]
Inze, Dirk [1 ,2 ]
Vanholme, Bartel [1 ,2 ]
Depuydt, Stephen [1 ,2 ,3 ,5 ]
机构
[1] Univ Ghent, Dept Plant Biotechnol & Bioinformat, Technol Pk 71, B-9052 Ghent, Belgium
[2] VIB Ctr Plant Syst Biol, Technol Pk 71, B-9052 Ghent, Belgium
[3] Univ Ghent, Lab Plant Growth Anal, Global Campus, Incheon, South Korea
[4] Univ Cambridge, Sainsbury Lab, Cambridge CB2 1LR, England
[5] HOGENT Univ Appl Sci & Arts, Dept Healthcare, B-9000 Ghent, Belgium
关键词
<italic>Arabidopsis</italic>; Auxin; Brassinosteroid; Coumarin; Hypocotyl; GENE-EXPRESSION; ROOT-FORMATION; BIOSYNTHESIS; TRANSPORT; MORPHOLOGY; INHIBITOR; TISSUE; POTENT;
D O I
10.1007/s00344-024-11617-z
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Coumarin is a bioactive molecule that impacts various plant developmental processes, including germination, root growth and shoot elongation. Despite the long-standing awareness of coumarin's effect on plant growth, its mode of action remains elusive. We investigated the capacity of coumarin to enhance hypocotyl elongation in light-grown Arabidopsis seedlings, demonstrating that this effect is mediated by the stimulation of cell elongation rather than cell division. Functional analyses revealed that the promotion of cell elongation occurs independently of ethylene and gibberellic acid, while emphasizing the critical roles of auxin and brassinosteroids in this process. The auxin dependency was evidenced by the reduced response to coumarin treatment in both the tir1-1/afb2-1/afb3-1 triple and slr-1 gain-of-function mutant. The persistence of coumarin's effects in the presence of yucasin suggests that de novo auxin biosynthesis is not essential for its activity. In contrast, brassinosteroid biosynthesis is critical as coumarin failed to restore the stunted hypocotyl phenotype when brassinosteroid biosynthesis was inhibited by propiconazole. Furthermore, the brassinosteroid receptor mutant bri1-116 exhibited insensitivity to coumarin and the bak1-4 signalling mutant showed a markedly diminished response, underscoring the necessity of both brassinosteroids and a functional brassinosteroid signalling pathway for coumarin-induced hypocotyl elongation.
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页数:14
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