Abstract
HKT channels are a plant protein family involved in sodium (Na+) and potassium (K+) uptake and Na+-K+ homeostasis. Some HKTs underlie salt tolerance responses in plants, while others provide a mechanism to cope with short-term K+ shortage by allowing increased Na+ uptake under K+ starvation conditions. HKT channels present a functionally versatile family divided into two classes, mainly based on a sequence polymorphism found in the sequences underlying the selectivity filter of the first pore loop. Physiologically, most class I members function as sodium uniporters, and class II members as Na+/K+ symporters. Nevertheless, even within these two classes, there is a high functional diversity that, to date, cannot be explained at the molecular level. The high complexity is also reflected at the regulatory level. HKT expression is modulated at the level of transcription, translation, and functionality of the protein. Here, we summarize and discuss the structure and conservation of the HKT channel family from algae to angiosperms. We also outline the latest findings on gene expression and the regulation of HKT channels.
Highlights
Classes I and II are differentiated by the presence of either a serine residue (SGGG) or a glycine residue (GGGG) in the first pore loop, which mostly translates into class-specific differences in ion conduction [7]
High functional variability of HKT channels and other transporters involved in the Na+ and K+ homeostasis demonstrates the complexity and diversity of Na+ detoxification and usage strategies
HKT proteins are regulated on many levels, including transcriptional and translational levels, and directly at the protein level
Summary
Classes I and II are differentiated by the presence of either a serine residue (SGGG) or a glycine residue (GGGG) in the first pore loop, which mostly translates into class-specific differences in ion conduction [7]. Exceptions to this classification have been found, questioning the classification’s accuracy [5,8,9,10,11]. The Na+-K+ symport ability is advantageous under conditions of K+ starvation due to the capacity of Na+ to functionally replace K+ to a certain extent, bridging the short-term lack of K+ and ensuring the survival of the plant [36] This is in line with the previously described upregulation of HKT transcripts under K+ shortage.
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