MYB42 inhibits hypocotyl cell elongation by coordinating brassinosteroid homeostasis and signalling in Arabidopsis thaliana. (18th December 2021)

• Record Type: Journal Article
• Authors: Zhuang, Yamei; Lian, Wenjun; Tang, Xianfeng; Qi, Guang; Wang, Dian; Chai, Guohua; Zhou, Gongke
• Is Part Of: Annals of botany. Volume 129:Number 4(2022)
• Page Start: 403
• Page End: 413
• Publication Date: 2021-12-18
• Subjects: Hypocotyl elongation -- MYB transcription factor -- BR homeostasis and signalling -- feedback regulation -- DOGT1/UGT73C5 -- Arabidopsis thaliana; Botany -- Periodicals; 580
• DOI: 10.1093/aob/mcab152
• Languages: English
• ISSNs: 0305-7364

Abstract

Abstract: Background and Aims: The precise control of brassinosteroid (BR) homeostasis and signalling is a prerequisite for hypocotyl cell elongation in plants. Arabidopsis MYB42 and its paralogue MYB85 were previously identified to be positive regulators of secondary cell wall formation during mature stages. Here, we aim to reveal the role of MYB42 and MYB85 in hypocotyl elongation during the seedling stage and clarify how MYB42 coordinates BR homeostasis and signalling to regulate this process. Methods: Histochemical analysis of proMYB42-GUS transgenic plants was used for determination of the MYB42 expression pattern. The MYB42, 85 overexpression, double mutant and some crossing lines were generated for phenotypic observation and transcriptome analysis. Transcription activation assays, quantitative PCR (qPCR), chromatin immunoprecipitation (ChIP)-qPCR and electrophoretic mobility shift assays (EMSAs) were conducted to determine the relationship of MYB42 and BRASSINAZOLE-RESISTANT 1 (BZR1), a master switch activating BR signalling. Key Results: MYB42 and MYB85 redundantly and negatively regulate hypocotyl cell elongation. They function in hypocotyl elongation by mediating BR signalling. MYB42 transcription was suppressed by BR treatment or in bzr1-1D (a gain-of-function mutant of BZR1), and mutation of both MYB42 and MYB85 enhanced the dwarf phenotype of the BR receptor mutant bri1-5 . BZR1 directly repressed MYB42 expression in response to BR. Consistently, hypocotyl length of bzr1-1D was increased by simultaneous mutation of MYB42 and MYB85, but was reduced by overexpression of MYB42 . Expression of a number of BR-regulated BZR1 (non-)targets associated with hypocotyl elongation was suppressed by MYB42, 85. Furthermore, MYB42 enlarged its action in BR signalling through feedback repression of BR accumulation and activation of DOGT1/UGT73C5, a BR-inactivating enzyme. Conclusions: MYB42 inhibits hypocotyl elongation by coordinating BR homeostasis and signalling during primary growth. The present study shows an MYB42, 85-mediated multilevel system that contributes to fine regulation of BR-induced hypocotyl elongation.