Wang P, Guo Q, Wang Q, Zhou XR, Wang SM*.PtAKT1 maintains selective absorption capacity for K⁺ over Na⁺in halophyte Puccinellia tenuiflora under salt stress. Acta Physiologiae Plantarum. 2015 Doi: 10.1007/s11738-015-1846-3. http://link.springer.com/article/10.1007/s11738-015-1846-3 

摘要：

The halophyte Puccinellia tenuiflora efficiently restricts Na⁺ entry into roots and maintains a strong selective absorption (SA) capacity for K⁺ over Na⁺ to cope with salt stress. AKT1-type channel, an important plant K⁺ uptake protein, may be active in regulating SA in P. tenuiflora. Here, its encoding gene PtAKT1 was isolated from P. tenuiflora. To examine the function of PtAKT1 in salt resistance and selectivity for K⁺ over Na⁺, we analyzed the transcript patterns of PtAKT1 and Na⁺, K⁺concentration in P. tenuiflora during varying concentrations of NaCl and KCl. Results displayed that both the transcription abundance of PtAKT1 in roots and the whole plant K⁺ concentration did not change with varying K⁺ concentrations in the medium (0-10 mM). When NaCl (25 or 150 mM) was present, transcript levels of PtAKT1 were down-regulated, accompanied by a decrease in the whole plant K⁺ concentration. However, under normal (5 mM) or low (0.1 mM) KCl condition, transcript levels of PtAKT1 in roots under severe salt stress (150 mM NaCl) were higher than that in mild salt condition (25 mM NaCl) within 6?24 h, so did SA during the whole treatment time (6?96 h). A strong positive correlation was existed between root PtAKT1 transcription abundance and SA values during 25 or 150 mM NaCl plus KCl. Consequently, it is proposed that PtAKT1 is a key factor in regulating selective absorption capacity for K⁺ over Na⁺ in P. tenuiflora during saline condition. Finally, we hypothesize a model that SOS1, HKT and SKOR synergistically regulate potassium and sodium transport systems in the xylem parenchyma, and subsequently modulates K⁺ absorption via AKT1, which is located in epidermis, cortex and endodermis. The model could also provide a likely evidence to the mechanism that SOS1 could protect AKT1 mediating K⁺ influx during salt stress.