A Ca2+-Sensitive System Mediates Low-Affinity K+ Uptake in the Absence of AKT1 in Arabidopsis Plants
A Ca2+-Sensitive System Mediates Low-Affinity K+ Uptake in the Absence of AKT1 in Arabidopsis Plants
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DOI：
10.1093/pcp/pcs140
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发表时间：
2012-12-01
影响因子：
4.9
通讯作者：
Rubio, Francisco
中科院分区：
文献类型：
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作者：
Caballero, Fernando;Botella, Maria A.;Rubio, Francisco
拟南芥根对K+的吸收主要由高亲和力K+转运蛋白AtHAK 5和内向整流钾通道AtAKT 1介导。这种模式对植物来说可能是普遍的。缺乏这两个系统（athak 5，atakt 1）的突变体植物采取K+和生长时，外部K+浓度高于一定水平，表明一个额外的运输系统可能会补偿AtHAK 5和AtAKT 1的情况。在这里，我们描述了这种替代系统是必不可少的，提供足够的K+，以维持生长的athak 5，atakt 1植物。该系统对Ca ~（2+）、Mg ~（2+）、Ba ~（2+）、La ~（3+）等离子特别敏感，能转运Cs ~+，环核苷酸能降低其活性。这些结果表明，钙渗透的电压非依赖性非选择性阳离子通道，可能属于环核苷酸门控通道（CNGC）的家庭，可能提供了途径的K+吸收在athak 5，atakt 1植物。编码已被描述为介导根K+吸收的CNGC家族的两个成员AtCNGC 3和AtCNGC 10的基因在atak 5、atakt 1植物中不上调，排除这些基因作为补偿机制的过表达。另一方面，由于其根细胞的膜电位的超极化，在athak 5，atakt 1植物中K+的驱动力增加也被丢弃。这种未知系统的识别可能提供工具，以改善植物K+营养的条件下，AtAKT 1功能降低，如在盐度。此外，该系统可能构成一个重要的途径，积累有毒的阳离子，如Cs+或放射性铯（Cs-137（+）），并可能在植物修复中发挥作用。
K+ acquisition by Arabidopsis roots is mainly mediated by the high-affinity K+ transporter AtHAK5 and the inward-rectifier K+ channel AtAKT1. This model is probably universal to plants. Mutant plants lacking these two systems (athak5,atakt1) take up K+ and grow when the external K+ concentration is above a certain level, indicating that an additional transport system may compensate for the absence of AtHAK5 and AtAKT1. Here we describe that this alternative system is essential for providing sufficient K+ to sustain growth of athak5,atakt1 plants. This system is especially sensitive to Ca2+, Mg2+, Ba2+ and La3+, it transports Cs+ and its activity is reduced by cyclic nucleotides. These results suggest that a Ca2+-permeable voltage-independent non-selective cation channel, probably belonging to the cyclic nucleotide gated channel (CNGC) family, may provide the pathway for K+ uptake in athak5,atakt1 plants. The genes encoding the two members of the CNGC family that have been described as mediating root K+ uptake, AtCNGC3 and AtCNGC10, are not up-regulated in athak5,atakt1 plants, excluding overexpression of these genes as a compensatory mechanism. On the other hand, an increased driving force for K+ in athak5,atakt1 plants due to a hyperpolarization of the membrane potential of its root cells is also discarded. The identification of this unknown system may provide tools to improve plant K+ nutrition in conditions where AtAKT1 functionality is reduced, such as under salinity. In addition, this system may constitute an important pathway for accumulation of toxic cations such as Cs+ or radiocesium (Cs-137(+)), and could play a role in phytoremediation.