Recent Advances in Understanding the Regulatory Mechanism of Plasma Membrane H+-ATPase through the Brassinosteroid Signaling Pathway
- PMID: 38372617
- DOI: 10.1093/pcp/pcae014
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 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.
Keywords: BAK1; BIN2; BRI1; Brassinosteroids; Plasma membrane H+-ATPase; SAUR.
© The Author(s) 2024. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site–for further information please contact journals.permissions@oup.com.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
