Title: ZxAKT1 is essential for K⁺ uptake and K⁺/Na⁺ homeostasis in the succulent xerophyte Zygophyllum xanthoxylum

Authors: Qing Ma, Jing Hu, Xiang-Rui Zhou, Hui-Jun Yuan, Tanweer Kumar, Sheng Luan, Suo-Min Wang*

Journal: The Plant Journal

Impact Factor: 5.468

Abstract: The inward-rectifying K⁺ channel AKT1 constitutes an important pathway for K⁺ acquisition in plant roots. In glycophytes, excessive accumulation of Na⁺ is accompanied by K⁺ deficiency under salt stress. However, in the succulent xerophyte Zygophyllum xanthoxylum, which exhibits excellent adaptability to adverse environments, K⁺ concentration remains at a relatively constant level despite increased levels of Na⁺ under salinity and drought conditions. In this study, the contribution of ZxAKT1 to maintaining K⁺ and Na⁺ homeostasis in Z. xanthoxylum was investigated. Expression of ZxAKT1 rescued the K⁺-uptake-defective phenotype of yeast strain CY162, suppressed the salt-sensitive phenotype of yeast strain G19, and complemented the low-K⁺-sensitive phenotype of Arabidopsis akt1 mutant, indicating that ZxAKT1 functions as an inward-rectifying K⁺ channel. ZxAKT1 was predominantly expressed in roots, and was induced under high concentrations of either KCl or NaCl. By using RNA interference technique, we found that ZxAKT1-silenced plants exhibited stunted growth compared to wild-type Z. xanthoxylum. Further experiments showed that ZxAKT1-silenced plants exhibited a significant decline in net uptake of K⁺ and Na⁺, resulting in decreased concentrations of K⁺ and Na⁺, as compared to wild-type Z. xanthoxylum grown under 50 mM NaCl. Compared with wild-type, the expression levels of genes encoding several transporters/channels related to K⁺/Na⁺ homeostasis, including ZxSKOR, ZxNHX, ZxSOS1 and ZxHKT1;1, were reduced in various tissues of a ZxAKT1-silenced line. These findings suggest that ZxAKT1 not only plays a crucial role in K⁺ uptake but also functions in modulating Na⁺ uptake and transport systems in Z. xanthoxylum, thereby affecting its normal growth.

链接：http://onlinelibrary.wiley.com/doi/10.1111/tpj.13465/full