K+ Efflux Antiporters 4, 5, and 6 Mediate pH and K+ Homeostasis in Endomembrane Compartments
K+ Efflux Antiporters 4, 5, and 6 Mediate pH and K+ Homeostasis in Endomembrane Compartments
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K 外流逆向转运蛋白 4、5 和 6 调节内膜区室中的 pH 和 K 稳态
DOI：
10.1104/pp.18.01053
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发表时间：
2018
期刊：
影响因子：
7.4
通讯作者：
Qiu QS
中科院分区：
文献类型：
--
作者：
Zhu X;Pan T;Zhang X;Fan L;Quintero FJ;Zhao H;Su X;Li X;Villalta I;Mendoza I;Shen J;Jiang L;Pardo JM;Qiu QS
KEA4、KEA5和KEA6是拟南芥K+外排逆向转运蛋白(KEA)家族的成员，具有很高的序列相似性，但其功能尚不清楚。KEA4、KEA5和KEA6具有相似的组织表达模式，并且这三种KeA蛋白定位于高尔基体、跨高尔基体和腺泡前室/多囊小体，提示这些蛋白在内膜系统中的作用是重叠的。单、双和三个突变体的表型分析证实了功能冗余。三变株KAA4KAA5KAA6莲座率小，幼苗短，对低K+有效性和高盐碱度敏感。此外，与KeA蛋白的K/H交换活性相一致，kea4kea5kea6突变体植株高尔基体、跨高尔基体网络、叶前隔室和液泡的管腔pH降低。遗传分析表明，KEA4、KEA5和KEA6以及内体Na+/H+交换器5(NHX5)和NHX6协同作用促进内体pH动态平衡和耐盐性。在kea4-kea5-kea6突变背景中，既不取消也不过度表达液泡反转录因子NHX1和NHX2，都不会改变盐敏感的表型。Kea4kea5kea6突变背景中的NHX1和NHX2蛋白不能抑制内膜系统的酸性，但使液泡的pH值接近野生型。综上所述，这些数据表明KEA4、KEA5和KEA6是内体K+转运体，功能是维持内膜网络的pH和离子动态平衡。
KEA4, KEA5, and KEA6 are members of the Arabidopsis (Arabidopsis thaliana) K+efflux antiporter (KEA) family that share high sequence similarity but whose function remains unknown. Here, we show their gene expression pattern, subcellular localization, and physiological function in Arabidopsis.KEA4,KEA5, andKEA6had similar tissue expression patterns, and the three KEA proteins localized to the Golgi, the trans-Golgi network, and the prevacuolar compartment/multivesicular bodies, suggesting overlapping roles of these proteins in the endomembrane system. Phenotypic analyses of single, double, and triple mutants confirmed functional redundancy. The triple mutantkea4 kea5 kea6had small rosettes, short seedlings, and was sensitive to low K+availability and to the sodicity imposed by high salinity. Also, thekea4 kea5 kea6mutant plants had a reduced luminal pH in the Golgi, trans-Golgi network, prevacuolar compartment, and vacuole, in accordance with the K/H exchange activity of KEA proteins. Genetic analysis indicated that KEA4, KEA5, and KEA6 as well as endosomal Na+/H+exchanger5 (NHX5) and NHX6 acted coordinately to facilitate endosomal pH homeostasis and salt tolerance. Neither cancelling nor overexpressing the vacuolar antiportersNHX1andNHX2in thekea4 kea5 kea6mutant background altered the salt-sensitive phenotype. The NHX1 and NHX2 proteins in thekea4 kea5 kea6mutant background could not suppress the acidity of the endomembrane system but brought the vacuolar pH close to wild-type values. Together, these data signify that KEA4, KEA5, and KEA6 are endosomal K+transporters functioning in maintaining pH and ion homeostasis in the endomembrane network.