a. Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou, Gansu 730000, China;
b. Key Laboratory of Gene Editing for Breeding, School of Life Sciences, Lanzhou University, Lanzhou, Gansu 730000, China;
c. Science and Research Department, College of Life Sciences, Northwest Normal University, Lanzhou, Gansu 730070, China;
d. Academy of Plateau Science and Sustainability, Qinghai Normal University, Xining, Qinghai 810016, China;
e. School of Life Sciences, Guangzhou University, Guangzhou, Guangdong 510006, China
Funds:
This study was supported by the National Natural Science Foundation of China (32370295 and 32170280 to K.H.), Foundation of Science and Technology of Gansu Province (22ZD6NA049). the Fundamental Research Funds for the Central Universities (lzujbky-2021-kb05 to Y.F., and lzujbky-2023-kb05 to P.L.), the Science and Technology Department of Gansu Province (24JRRA392 to K.H., 23JRRA1132 to C.X.), China Postdoctoral Science Foundation (2024M751259, GZB20240285 to B.L.), and Science and Technology Program of Gansu Province (25JRRA718 to B.L.)
Brassinosteroids (BRs) are essential phytohormones that broadly regulate plant growth, development, and adaptation to biotic and abiotic stresses. In Arabidopsis, apoplastic BR molecules are perceived by a plasma membrane-localized receptor complex comprising the ligand-binding receptor BRI1 and the co-receptor BAK1. While negative regulators of the BR receptor complex, such as BKI1, BIR3, and PUB12/13, have been well characterized, how BRI1 and BAK1 are positively modulated in the BR pathway remains largely unknown. In this study, a genetic screen involving overexpression of RLP genes in the bak1-3 bkk1-1 double mutant reveals that enhanced RLP51 expression partially suppresses the BR-deficient phenotypes of bak1-3 bkk1-1. RLP51 overexpression also partially rescues the weak bri1 mutant allele, bri1-301. Although the rlp51 single mutant exhibits wild-type-like phenotypes, it enhances BR-defective phenotypes in bri1-301 and bak1 serk1 mutants. RLP51 is next found to interact with both BRI1 and BAK1 without affecting BRI1-BAK1 interaction. Critically, co-expression of RLP51 with BRI1 or BAK1 significantly increases BRI1 and BAK1 protein abundances. RLP51 appears to promote protein synthesis rather than stabilize BRI1 and BAK1 proteins. Thus, our study identifies RLP51 as a positive regulator of BR signaling that enhances the protein levels of BRI1 and BAK1.
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