Arabidopsis Ankyrin-Repeat Protein Kinase ANK-PK2 Negatively Regulates Salt Tolerance by Mediating Degradation of the Sugar Transporter Protein STP11.

IF 6 1区 生物学 Q1 PLANT SCIENCES Plant, Cell & Environment Pub Date : 2025-01-30 DOI:10.1111/pce.15417
Qijun Ma, Shuo Xu, Shi Hu, Kaijing Zuo
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Abstract

Soluble sugars provide energy sources required for plant growth and development. They also act as osmoprotectants to improve the salt tolerance of plants. However, molecular mechanism underlying the negative regulation of soluble sugar accumulation in plants under salt stress conditions remains unknown. In this study, we investigated the functions of ankyrin-repeat kinase 2 (ANK-PK2) that regulates soluble sugar content in Arabidopsis under salt stress. ANK-PK2 interacts with and phosphorylates the sugar transporter protein 11 (STP11) under salt stress. Phosphorylated STP11 is easier to degrade, and its glucose-transporting ability and soluble sugar accumulation are inhibited. The ank-pk2 mutant exhibited increased salt tolerance. The salt-sensitive phenotype of the mutant stp11 was recovered through a dephosphorylation mutation that changed Thr227 in STP11 to Ala227. Our results revealed a novel molecular mechanism underlying salt stress adaptation in Arabidopsis, which ANK-PK2 negatively regulates salt tolerance by phosphorylating and subsequently decreasing the transport activity of STP11 to balance the cellular soluble sugar content in Arabidopsis.

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来源期刊
Plant, Cell & Environment
Plant, Cell & Environment 生物-植物科学
CiteScore
13.30
自引率
4.10%
发文量
253
审稿时长
1.8 months
期刊介绍: Plant, Cell & Environment is a premier plant science journal, offering valuable insights into plant responses to their environment. Committed to publishing high-quality theoretical and experimental research, the journal covers a broad spectrum of factors, spanning from molecular to community levels. Researchers exploring various aspects of plant biology, physiology, and ecology contribute to the journal's comprehensive understanding of plant-environment interactions.
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