Recent Advances in Understanding the Regulatory Mechanism of Plasma Membrane H+-ATPase through the Brassinosteroid Signaling Pathway

Abstract The polyhydroxylated steroid phytohormone brassinosteroid (BR) controls many aspects of plant growth, development and responses to environmental changes. Plasma membrane (PM) H+-ATPase, the well-known PM proton pump, is a central regulator in plant physiology, which mediates not only plant...

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Veröffentlicht in:Plant and cell physiology 2024-11, Vol.65 (10), p.1515-1529
Hauptverfasser: Lin, Zhaoheng, Zhu, Pan, Gao, Liyang, Chen, Xuanyi, Li, Meijing, Wang, Yuhe, He, Junxian, Miao, Ying, Miao, Rui
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Sprache:eng
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Zusammenfassung:Abstract The polyhydroxylated steroid phytohormone brassinosteroid (BR) controls many aspects of plant growth, development and responses to environmental changes. Plasma membrane (PM) H+-ATPase, the well-known PM proton pump, is a central regulator in plant physiology, which mediates not only plant growth and development, but also adaptation to stresses. Recent studies highlight that PM H+-ATPase is at least partly regulated via the BR signaling. Firstly, the BR cell surface receptor BRASSINOSTEROID-INSENSITIVE 1 (BRI1) and multiple key components of BR signaling directly or indirectly influence PM H+-ATPase activity. Secondly, the SMALL AUXIN UP RNA (SAUR) gene family physically interacts with BRI1 to enhance organ development of Arabidopsis by activating PM H+-ATPase. Thirdly, RNA-sequencing (RNA-seq) assays showed that the expression of some SAUR genes is upregulated under the light or sucrose conditions, which is related to the phosphorylation state of the penultimate residue of PM H+-ATPase in a time-course manner. In this review, we describe the structural and functional features of PM H+-ATPase and summarize recent progress towards understanding the regulatory mechanism of PM H+-ATPase by BRs, and briefly introduce how PM H+-ATPase activity is modulated by its own biterminal regions and the post-translational modifications.
ISSN:0032-0781
1471-9053
1471-9053
DOI:10.1093/pcp/pcae014