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Botanical Research

2168-5665

Scientific Research Publishing

10.12677/BR.2020.96068

BR-38853

BR20200600000_18441810.pdf

生命科学

植物响应低钾胁迫的信号传导和分子调节机制的研究进展 Research Progress on Signal Transduction and Molecular Regulatory Mechanism of Plants in Response to Low K ⁺Stress

王

茜

¹ ^* 刘

欣

¹ ² 姜

晶

¹ ²

沈阳农业大学园艺学院，辽宁沈阳

null

14 10 2020

09 06 551 560

2014

This work is licensed under the Creative Commons Attribution International License (CC BY). http://creativecommons.org/licenses/by/4.0/

钾离子在植物生长发育的诸多生理生化过程中起重要作用。由于连续的耕种和肥料的不合理使用，土壤钾离子含量日益下降。钾离子的缺乏已经成为限制植物正常生长发育的主要因子之一。因此，培育耐低钾品种已经成为重要的育种目标，耐低钾分子机制的研究和相关基因的挖掘对植物耐低钾品种改良奠定了基础。为了在低钾环境下生存，植物形成了复杂而高效的低钾信号传导途径，并且结合转录和翻译后调节机制协同抵御低钾胁迫。本文结合前人研究，主要从低钾信号的传递、转录水平调控和翻译后调控这三方面讨论了植物耐低钾的分子机制，为植物耐低钾的遗传改良提供了分子理论依据，也为今后的耐低钾研究提供一定的思路。 K⁺plays crucial roles in diverse physiological and biochemical processes during plant growth and development. Due to irrational use of fertilizer and continuous cultivate, the K⁺content of soil de-creased gradually. Deficiency of K⁺content has become one of the major factors limiting the growth and development of plant. Therefore, breeding low K⁺-resistant varieties has become an important target of current crop breeding, and the excavation of low K⁺-resistant genes will lay the foundation for the variety improvement of low K⁺resistance. To survive in low K+ environment, plants have evolved complex and high-efficiency signal transduction pathway, and combined with transcrip-tional regulatory and post-translational regulation to resist to low K⁺stress. This paper, combined the previous research, discussed the molecular mechanism of low K⁺tolerance from three aspects of low K⁺signal transduction pathway, transcriptional regulatory and post-translational regulation to provide a molecular theoretical basis for genetic improvement of plant low K⁺tolerance and a direc-tion for the study of plant low K⁺resistance in the future.

低钾胁迫，低钾信号传导，转录调节，翻译后调控，分子机制, Low K ⁺Stress Low KK ⁺Signal Transduction Transcriptional Regulatory Post-Translational Regulation Molecular Mechanism

摘要

关键词

低钾胁迫，低钾信号传导，转录调节，翻译后调控，分子机制

Research Progress on Signal Transduction and Molecular Regulatory Mechanism of Plants in Response to Low K+ Stress

Xi Wang, Xin Liu, Jing Jiang^*

College of Horticulture, Shenyang Agricultural University, Shenyang Liaoning

Received: Oct. 23^rd, 2020; accepted: Nov. 20^th, 2020; published: Nov. 27^th, 2020

ABSTRACT

K⁺plays crucial roles in diverse physiological and biochemical processes during plant growth and development. Due to irrational use of fertilizer and continuous cultivate, the K⁺content of soil decreased gradually. Deficiency of K⁺content has become one of the major factors limiting the growth and development of plant. Therefore, breeding low K⁺-resistant varieties has become an important target of current crop breeding, and the excavation of low K⁺-resistant genes will lay the foundation for the variety improvement of low K⁺resistance. To survive in low K⁺environment, plants have evolved complex and high-efficiency signal transduction pathway, and combined with transcriptional regulatory and post-translational regulation to resist to low K⁺stress. This paper, combined the previous research, discussed the molecular mechanism of low K⁺tolerance from three aspects of low K⁺signal transduction pathway, transcriptional regulatory and post-translational regulation to provide a molecular theoretical basis for genetic improvement of plant low K⁺tolerance and a direction for the study of plant low K⁺resistance in the future.

Keywords:Low K⁺Stress, Low K⁺Signal Transduction, Transcriptional Regulatory, Post-Translational Regulation, Molecular Mechanism

This work is licensed under the Creative Commons Attribution International License (CC BY 4.0).

http://creativecommons.org/licenses/by/4.0/

1. 引言

钾离子是植物中重要的大量元素之一，在植物生长发育过程中扮演着重要角色，钾离子具有丰富的生理生化功能，包括维持细胞渗透压平衡、保障酶活性、优化光合性能、促进同化产物运输等 [ 1 ]。近年来，随着我国作物产量的提高，农田土壤出现钾素亏缺现象 [ 2 ]。钾离子短时间的缺乏会造成植株根毛伸长和根部生长受限 [ 3 ] [ 4 ] [ 5 ]，而随着缺钾时间的延长，会使植物叶片发生黄化和植株整体生长受到抑制 [ 6 ] [ 7 ] [ 8 ]，最后造成质量和产量的严重损失。

低钾胁迫下，植物首先会感应到低钾信号并将信号传递至细胞内，信号可以被传导并随后触发下游响应从而启动一些耐低钾相关基因的表达，随后会造成植物的表型发生一些变化，最终促进植物适应缺钾的环境 [ 9 ]。在这个过程中，信号传导、转录调控和翻译后调节发挥着重要作用。近年来，有关植物耐低钾的研究，特别是响应低钾胁迫的分子机制得到了广泛的关注，本文就这方面取得的进展进行总结，为低钾胁迫分子机制的下一步研究奠定基础。

2. 低钾胁迫信号转导途径 2.1. Ca2+通道信号传导

低钾胁迫首先对质膜产生影响，激活Ca²⁺通道，从而启动Ca²⁺信号传导通路(图1)。植物在遭受低钾胁迫时，Ca²⁺传感器钙调磷酸酶B类蛋白CBL (calcineurin B-like protein)可以与特定的蛋白激酶CIPK (CBL-interacting kinase)相互作用，形成复合体去传递Ca²⁺信号，激活耐低钾相关基因，从而响应低钾胁迫。高亲和性钾转运蛋白HAK5和钾离子通道AKT1是目前研究较多的两个耐低钾基因，在拟南芥中已发现CBL1-CIPK23-HAK5和CBL1/9-CIPK23-AKT1传导路径可以增加根部钾离子的吸收以响应低钾胁迫 [ 10 ] [ 11 ]。在水稻中也存在CBL1-CIPK23途径，传递信号激活AKT1通道，增加钾离子的吸收 [ 12 ]。此外，还发现了CIPK6和CIPK16也可以依赖CBLs方式传递低钾信号去激活AKT1 [ 13 ]。钾离子通道AKT2的活性也可以被CBL4-CIPK6信号调节 [ 14 ]。除了CBL-CIPK复合体协同传递低钾信号外，还发现CBL和CIPK之间存在竞争关系，CBL10可以不和CIPK23发生互作而直接传递低钾信号与AKT1一起调节植物钾离子稳态 [ 15 ]。最近的研究发现了在低钾胁迫下，拟南芥CIPK9和蛋白磷酸酶(protein phosphatase 2C, PP2C)家族成员AP2C1发生互作并且可以提高植物的低钾耐性，这暗示了PP2C也参与了Ca²⁺介导的低钾信号传导，但具体机制还不清楚 [ 16 ]。在不同的植物中这种Ca²⁺信号途径是不同的，即使在相同植物中也存在多条信号途径响应低钾，表明这种信号传递途径是高效且复杂的。

2.2. 植物激素信号传导

乙烯是可以响应低钾信号的，在拟南芥多个实验中均发现钾离子的缺乏可以导致乙烯的含量迅速的增加，随后诱导了活性氧(reactive oxygen species, ROS)含量的增加，调控HAK5表达量上调和根毛的伸长去响应低钾胁迫 [ 17 ] [ 18 ]。最新的研究也发现拟南芥可以通过乙烯信号途径增加根毛的伸长进而响应低钾胁迫 [ 3 ]。

在多个实验中均发现，低钾胁迫会通过影响生长素的含量来影响根部的生长，这暗示了生长素信号可能响应低钾胁迫 [ 19 ] [ 20 ] [ 21 ] [ 22 ]。钾转运蛋白KUP4可以通过调节生长素载体(auxin transporter, PIN1)的位置来影响钾依赖性根部形态的发育 [ 23 ] [ 24 ]。近期研究发现拟南芥AKT1可以感应低钾信号并且影响生长素的转运和分布和减少根尖的生长素含量，从而使根部停止生长 [ 20 ]。在番茄中也存在类似的根部生长素浓度下降的现象，但具体的信号传导途径还是未知的 [ 5 ]。

蛋白激酶SRK2E (SNF1-relatedprotein kinases 2E)是ABA信号途径的关键成分，有研究发现钾转运蛋白KUP6可以与SRK2E互作，通过ABA信号调节钾离子稳态和渗透调节以响应气孔开闭 [ 25 ]。此外，钾离子缺乏和ABA也可以诱导钾转运蛋白CHX17的表达，但具体机制还未清楚 [ 26 ]。这些都表明ABA可以感应低钾信号并且调节相关低钾基因抵御低钾胁迫。

茉莉酸是和非生物胁迫紧密相关的一种激素，有研究发现其响应低钾胁迫。在水稻和小麦中茉莉酸合成相关酶丰度可以受钾离子缺乏的诱导显著增加，并且同时也增加了植物的低钾耐性 [ 27 ]，这也暗示了茉莉酸参与了低钾信号传导。茉莉酸信号也可以调节钾转运蛋白OsCHX14的表达，从而调节开花过程中的钾离子稳态 [ 28 ]。

植物激素广泛地参与了低钾胁迫信号传导的过程，已知低钾可以诱导乙烯、茉莉酸和ABA相关基因转录的增加，生长素含量的减少。最近的番茄转录组分析发现，除了这四种激素外，赤霉素，细胞分裂素以及水杨酸相关基因的转录水平在低钾处理前后均发生显著性变化 [ 5 ]。这暗示了在植物中多种激素均参与低钾信号传导(图1)，但大多的信号转导途径还是未知的。

2.3. microRNA途径

microRNA在植物发育调控、逆境应答及激素调节等方面发挥重要作用。目前microRNA在N、P、S和Cu营养缺乏实验中研究更为深入，在钾缺乏实验中研究是较少的。水稻OsmiR399可以通过调节多种营养元素的吸收响应缺素胁迫，过表达OsmiR399使植物体内各种营养元素含量上升，而钾离子缺乏可以诱导OsmiR399的表达并抑制其下游靶标基因LTN1/OsPHO2，随后上调钾转运蛋白OsHAK25的表达以响应低钾胁迫 [ 29 ]。在番茄中通过对microRNA进行测序发现存在7个差异表达的的microRNA响应低钾胁迫，并且提出了microRNA156与靶基因SPL3之间可能存在负调控关系响应低钾 [ 30 ]。miR168a也是一个被验证响应低钾的microRNA，miR168a过表达番茄植株在低钾处理后根毛与根面积显著增加 [ 31 ]。因此，microRNA是可以响应低钾信号，并将信号传递给特定的靶基因，最后调节耐低钾相关基因的表达(图1)。

2.4. ROS途径传导

当植物处在逆境胁迫下时会产生大量的活性氧，它是细胞内重要的信号分子。有研究显示，ROS不仅参与低钾信号传导，也是钙传导信号的上游调节子 [ 13 ] [ 32 ]。在拟南芥中发现低钾胁迫也诱导根部ROS的含量增加，并且ROS信号可以诱导HAK5去响应低钾胁迫 [ 17 ]。在番茄中也发现了相似的现象，在低钾处理后低钾敏感型植株的根和叶中ROS的浓度会显著上升，但具体的机制还不清楚 [ 5 ]。此外，低钾胁迫也诱导了一些ROS相关的酶含量的上升。RCI3 (type III peroxidase)是过氧化物酶家族的成员，低钾处理会增加其含量，其过表达也会增加ROS含量和HAK5的表达 [ 33 ]。同样地，与ROS产生有关的氧化酶NADPH (nicotinamide adenine dinucleotide phosphate)也会被低钾诱导，当抑制NADPH表达时会下调一些响应低钾胁迫的基因，例如HAK5和KEA5 [ 34 ]。由此可以发现，ROS的变化是响应钾离子缺乏的重要表现，RCI3和NADPH可能是ROS响应低钾信号途径的重要成员，并且均与HAK5相关。

图1. 植物低钾信号传导途径

3. 转录水平调节

植物面对较大的钾离子波动时，是依靠钾离子吸收和转运系统来进行调节的，这些钾离子吸收转运基因的转录调控是响应钾离子缺乏的普遍机制 [ 7 ]。在多种植物中均发现低钾胁迫会诱导一些钾离子转运蛋白基因的转录水平上调(图2)。在水稻中发现低钾会引起OsHAK1和OsHAK5的转录上调，增加了根部钾离子的吸收能力 [ 6 ] [ 35 ]。在谷子中发现SiHAK1在低钾处理后表达量增强了12倍，并且表现出高亲和性钾离子吸收能力 [ 36 ]。在拟南芥中发现HAK5的表达受到了钾离子缺乏的诱导而上调了，并且根部钾离子的含量更高了 [ 37 ]。最近在玉米中也发现了ZmHAK1在低钾处理下表达水平上升了 [ 4 ]。而这些受低钾诱导的基因的转录调控往往是依赖转录因子实现的，但具体的调节机制目前的发现的还是较少的。也存在一些钾转运蛋白的转录水平并不受低钾调控，例如KUP7的表达量在低钾处理后并未发生改变，KUP7过表达植株在低钾下也并未显示出低钾耐性 [ 7 ]，这暗示了KUP7可能是受到了翻译水平或翻译后水平的调节。

乙烯转录因子是植物响应和抵抗低钾胁迫主要的调控因子，在植物响应低钾胁迫的转录调节网络中扮演着重要作用。早期就有实验发现了低钾可以诱导拟南芥乙烯含量的增加，同时也可以诱导HAK5的转录水平和根毛的伸长，但具体机制并不清楚 [ 17 ]。后期研究发现乙烯可以诱导乙烯转录因子RAP2.11可以结合HAK5的启动子，调节其转录水平 [ 18 ]。在番茄中通过对低钾胁迫前后的转录组进行分析也发现了19个乙烯转录因子响应低钾胁迫 [ 5 ]。在最近的研究中也揭示了拟南芥在钾离子缺乏下，转录因子ZFP5 (zinc finger protein 5)通过调控乙烯信号途径中的EIN2 (ethyleneinsensitive 2)的转录，从而延长根毛的伸长去吸收更多钾离子 [ 3 ]。

此外，一些其他类型的转录因子也可以调节HAK5的转录。早期研究发现拟南芥在钾离子充足时，生长素相关转录因子ARF2 (auxinresponse factor 2)与HAK5的启动子结合抑制其表达，在低钾下ARF2被磷酸化解除了对HAK5的抑制作用，从而增加钾离子的吸收和根系的伸长 [ 38 ]。除了ARF2之外，也发现了转录因子DDF2 (dwarf and delayed flowering 2)、JLO (jagged lateral organs)、TFII_A (transcription initiation factor II_A gamma chain)和bHLH121 (basic helix-loop-helix 121)均可以在低钾胁迫下激活HAK5的启动子，从而获得更多的钾离子，使植株的耐低钾性更强 [ 39 ]。这些也展示出在低钾下，增加高亲和性转运蛋白HAK5的转录水平不仅可以提高钾离子的吸收还可以增强根部的伸长，从而缓解植物低钾性状。

此外，一些其他钾转运蛋白基因也被发现其在转录水平受转录因子调节。拟南芥NRT1.5/NPF7.3钾转运蛋白负责平衡根部和冠部钾离子的分布 [ 40 ]，有研究发现myb59和npf7.3突变体表现出相似的冠部发黄的现象，并且证明了转录因子MYB59 (v-myb avian myeloblastosis viral oncogene homolog 59)响应低钾调控，可以直接与NRT1.5/NPF7.3的启动子结合来调控其转录水平以响应低钾胁迫 [ 41 ]。在谷子中，转录因子SiNAC45 (nascent polypeptide-associated complex 45)也可以响应低钾胁迫和ABA的诱导，同时也增加了AKT1和HAK1的表达，并且在不同钾离子浓度下SiNAC45转基因植物具有不同的根长和根鲜重，但具体调节机制还不清楚 [ 42 ]。

图2. 植物响应低钾的转录调控

4. 翻译后调节

钾离子在维持细胞充盈和膜电位方面具有重要作用，钾离子的吸收和转运必须对环境变化做出快速反应，因此翻译后修饰调节非常重要(图3)。CBL-CIPK复合物是已知的植物耐低钾翻译后修饰调节的重要成分，其复合物可以在Ca²⁺信号下磷酸化低钾相关蛋白，增强植物耐低钾性。早期实验在爪蟾卵母细胞中验证了CIPK23、CIPK6和CIPK16和CBL1/2/3/9发生互作，这些CBL-CIPK复合物均可以激发AKT1的活性，其中CBL1-CIPK23复合物对AKT1的活性激发最强 [ 13 ]。拟南芥和水稻中也发现在低钾胁迫时CBL1-CIPK23可以磷酸化AKT1，进而促进植物钾离子的吸收能力和缓解了低钾胁迫性状 [ 11 ] [ 12 ]。在拟南芥中CBL1-CIPK23也可以磷酸化HAK5，激活HAK5去转运更多的钾离子 [ 10 ]。CBL除了可以和CIPK结合磷酸化AKT1外，还发现了CBL10与CIPK23发生了竞争作用，CBL10可以直接和AKT1的互作调节钾离子稳态 [ 15 ]。

此外，许多研究发现蛋白激酶PP2C可以与CBL和CIPK互作共同去调节耐低钾相关蛋白。AtAIP1是PP2C家族的一员，研究发现AIP1的去磷酸化AKT1与CBL1-CIPK23的磷酸化AKT1发生抵消作用，进而抑制AKT1介导的钾离子吸收活性 [ 13 ]。AtPP2CA是A型PP2C，其与CIPK6互作抑制CIPK6对AKT1的磷酸化，从而抑制AKT1的活性，然而同时又存在一些特定的CBLs可以与PP2CA发生物理作用去解除其抑制作用 [ 43 ]。可以发现PP2C往往是通过与CIPK发生竞争作用，进而负调节AKT1的活性。AtPP2CA还可以单独的影响钾离子通道AKT2，其去磷酸化AKT2抑制其活性 [ 44 ]。最近在拟南芥中发现PP2C家族的成员AP2C1可以去磷酸化CIPK9，并且在低钾下拟南芥ap2c1突变体的钾离子含量和根长相对于cipk9是更好的，这表明了在低钾胁迫下AP2C1充当负调节剂，CIPK9充当正调节剂，一起协调拟南芥的钾离子吸收和根部生长，但具体调节机制还未清楚 [ 16 ]。在植物中PP2C与CBL和CIPK之间存在复杂的互作关系，并且进而影响了钾离子通道，这形成了复杂的翻译后调节网络去响应低钾。

此外，也存在一些其他蛋白激酶具有翻译后调节作用。在拟南芥中编码Raf样MAPKK激酶的AtILK1 (integrin-linkedkinase 1)和钙调蛋白AtCML9 (calmodulin-like protein)结合与HAK5互作，促进HAK5在质膜上的积累，从而维持钾离子稳态 [ 45 ]。ABA信号相关蛋白激酶SRK2E也可以磷酸化KUP6调节钾离子

图3. 植物响应低钾的翻译后调控

稳态和气孔开闭 [ 25 ]。同样地，蔗糖相关蛋白激酶AtSnRK2.6 (SNF1-related protein kinase 2.6)也可以磷酸化KAT1从而调节气孔开闭和干旱胁迫 [ 46 ]。在番茄中也存在一些受体激酶(LRR-RLK)在低钾前后的转录水平发生显著性变化，暗示了这些受体激酶可能也参与了有低钾相关的一些翻译后调控 [ 5 ]。水稻中一个受体样激酶RUPO (receptor-like kinase)与钾转运蛋白OsHAK1/19/20互作，抑制其活性避免钾离子过度积累，从而介导花粉管生长和钾离子稳态 [ 47 ]。

此外，一些钙离子依赖性蛋白激酶CPKs (calcium-dependent protein kinases)，可以结合Ca²⁺并且具有激酶活性，它们通过磷酸化钾离子通道从而调节植物花粉管和气孔状态。AtCPK11和AtCPK24调控了花粉管钾离子通道AtSPIK去吸收钾离子，从而调节花粉管生长 [ 48 ]。在拟南芥中CPK13也可以磷酸化KAT1/2去调控气孔开放 [ 49 ]，CPK3/4/5/11/29可以磷酸化液泡钾离子通道TPK1 [ 46 ]。在非洲爪蟾卵母细胞中也验证了CPK33增强了shaker通道GORK的活性，并且影响了Ca²⁺依赖性的气孔开闭 [ 50 ]。

钾离子通道还可以在翻译后水平被一些通道亚基调节。AtKC1是shaker钾离子通道的亚基并且负调节剂钾离子通道的活性，单独并不发生作用 [ 51 ]。在拟南芥中发现AtKC1与AtAKT1相互作用形成AtAKT1-AtKC1异聚体通道，并在低钾下负调节AKT1吸收钾离子的活性和抑制根部生长 [ 52 ]。AtKC1也可以与AtCIPK23协同调节AtAKT1介导的低钾应激反应 [ 53 ]。钾离子通道KAT1和KC1还可以与囊泡相关膜蛋白VAMP721相互作用，在质膜上调节钾离子电流和根部的生长 [ 54 ]。此外，拟南芥阴离子通道SLAC1和SLAH3均可以通过蛋白互作直接抑制钾离子通道KAT1，从而调节气孔开放 [ 55 ]。

5. 展望

近年来植物耐低钾研究进展迅速，对模式植物耐低钾分子机理的研究不断加深。基因敲除、转基因植物和基因定位技术的应用推动了人们对耐低钾的深入研究，也为培育新的耐低钾品种提供了重要的理论依据。但是同时也存在一些问题，1) 低钾信号传导途径的开发还是不够完全的，还存在一些与胁迫相关的激素在低钾胁迫下的信号传导途径是未知的，例如细胞分裂素和赤霉素。另外，microRNA与低钾胁迫相关的研究也是较少的，这些都应作为未来的重点研究对象；2) HAK5的转录调节机制是目前研究的较多的，但还存在许多其他钾离子转运蛋白在低钾胁迫下转录水平也是上调的，例如OsHAK1、ZmHAK1和SiHAK1等，这些基因的转录水平上调的具体调节机制还是未知的。此外基因的转录后修饰研究目前是较少的，例如mRNA前体剪接加工、编辑、稳定性以及mRNA降解等，这些方面在未来可以进行深入研究；3) 耐低钾研究主要集中在拟南芥和水稻这种模式植物上，对于一些其他尚未进行基因组测序的植物研究甚少，低钾相关基因的功能研究十分受限。

致谢

本研究由国家重点研发项目(2019YFD100030)和国家自然科学基金项目(31801847)共同资助。

作者贡献

王茜负责撰写论文；刘欣负责文献资料的查找；姜晶是本综述的构思者及负责人，指导论文写作与修改。全体作者都阅读并同意最终的文本。

文章引用

王茜,刘欣,姜晶. 植物响应低钾胁迫的信号传导和分子调节机制的研究进展Research Progress on Signal Transduction and Molecular Regulatory Mechanism of Plants in Response to Low K⁺Stress[J]. 植物学研究, 2020, 09(06): 551-560. https://doi.org/10.12677/BR.2020.96068

参考文献

References 1

Li, W.H., Xu, G.H., Alli, A. and Yu, L. (2018) Plant HAK/KUP/KT K+Transporters: Function and Regulation. Seminars in Cell & Developmental Biology, 74, 133-141.
https://doi.org/10.1016/j.semcdb.2017.07.009

Tan, D., Jin, J., Jiang, L., Huang, S. and Liu, Z. (2012) Potassium Assessment of Grain Producing Soils in North China. Agriculture, Ecosystems and Environment, 148, 65-71.
https://doi.org/10.1016/j.agee.2011.11.016

Huang, L., Jiang, Q., Wu, J., An, L., Zhou, Z., Wong, C., Wu, M., Yu, H. and Gan, Y. (2020) Zinc Finger Protein 5 (ZFP5) Associates with Ethylene Signaling to Regulate the Phosphate and Potassium Deficiency-Induced Root Hair Development in Arabidopsis. Plant Molecular Biology, 102, 143-158.
https://doi.org/10.1007/s11103-019-00937-4

Qin, Y.J., Wu, W.H. and Wang, Y. (2019) ZmHAK5 and ZmHAK1 Function in K+ Uptake and Distribution in Maize under Low K+ Conditions. Journal of Integrative Plant Biology, 61, 691-705.
https://doi.org/10.1111/jipb.12756

Zhao, X.M., Liu, Y., Liu, X. and Jiang, J. (2018) Comparative Transcriptome Profiling of Two Tomato Genotypes in Response to Potassium-Deficiency Stress. International Journal of Molecular Sciences, 19, 2402.
https://doi.org/10.3390/ijms19082402

Chen, G., Hu, Q., Luo, L., Yang, T., Zhang, S., Hu, Y., Yu, L. and Xu, G. (2015) Rice Potassium Transporter OsHAK1 Is Essential for Maintaining Potassium-Mediated Growth and Functions in Salt Tolerance over Low and High Potassium Concentration Ranges. Plant, Cell & Environment, 38, 2747-2765.
https://doi.org/10.1111/pce.12585

Han, M., Wu, W., Wu, W.H. and Wang, Y. (2016) Potassium Transporter KUP7 Is Involved in K+ Acquisition and Translocation in Arabidopsis Root under K+-Limited Conditions. Molecular Plant, 9, 437-446.
https://doi.org/10.1016/j.molp.2016.01.012

Hu, W., Lu, Z., Meng, F., Li, X., Cong, R., Ren, T., Sharkey, T.D. and Lu, J. (2020) The Reduction in Leaf Area Precedes That in Photosynthesis under Potassium Deficiency: The Importance of Leaf Anatomy. New Phytologist, 227, 1749-1763.
https://doi.org/10.1111/nph.16644

Wang, Y. and Wu, W.H. (2017) Regulation of Potassium Transport and Signaling in Plants. Current Opinion in Plant Biology, 39, 123-128.
https://doi.org/10.1016/j.pbi.2017.06.006

Ragel, P., Ródenas, R., García-Martín, E. andrés, Z., Villalta, I., Nieves-Cordones, M., Rivero, R.M., Martínez, V., Pardo, J.M., Quintero, F.J. and Rubio, F. (2015) CIPK23 Regulates HAK5-Mediated High-Affinity K+ Uptake in Arabidopsis Roots. Plant Physiology, 169, 2863-2873.
https://doi.org/10.1104/pp.15.01401

Xu, J., Li, H.D., Chen, L.Q., Wang, Y., Liu, L.L., He, L. and Wu, W.H. (2006) A Protein Kinase, Interacting with Two Calcineurin B-Like Proteins, Regulates K+ Transporter AKT1 in Ara-bidopsis. Cell, 125, 1347-1360.
https://doi.org/10.1016/j.cell.2006.06.011

Li, J., Yu, L., Qi, G.N., Li, J., Xu, Z.J., Wu, W.H. and Yi, W. (2014) The OsAKT1 Channel Is Critical for K+ Uptake in Rice Roots and Is Modulated by the Rice CBL1-CIPK23 Complex. The Plant Cell, 26, 3387-3402.
https://doi.org/10.1105/tpc.114.123455

Lee, S.C., Lan, W.Z., Kim, B.G., Li, L., Cheong, Y.H., Pandey, G.K., Lu, G., Buchanan, B.B. and Luan, S. (2007) A Protein Phosphorylation/DephosphorylationNetwork Regulates a Plant Potassium Channel. Proceedings of the National Academy of Sciences of the United States of America, 104, 15959-15964.
https://doi.org/10.1073/pnas.0707912104

Held, K., Pascaud, F., Eckert, C., Gajdanowicz, P., Hashimoto, K., Corratgefaillie, C., Offenborn, J.N., Lacombe, B., Dreyer, I. and Thibaud, J.B. (2011) Calcium-Dependent Modulation and Plasma Membrane Targeting of the AKT2 Potassium Channel by the CBL4/CIPK6 Calcium Sensor/Protein Kinase Complex. Cell Research, 21, 1116-1130.
https://doi.org/10.1038/cr.2011.50

Ren, X.L., Qi, G.N., Feng, H.Q., Zhao, S., Zhao, S.S., Wang, Y. and Wu, W.H. (2013) Calcineurin B-Like Protein CBL10 Directly Interacts with AKT1 and Modulates K+Homeostasis in Ara-bidopsis. The Plant Journal, 74, 258-266.
https://doi.org/10.1111/tpj.12123

Singh, A., Yadav, A.K., Kaur, K., Sanyal, S.K., Jha, S.K., Fernandes, J.L., Sharma, P., Tokas, I., Pandey, A. and Luan, S. (2018) A Protein Phosphatase 2C, AP2C1, Interacts with and Negatively Regulates the Function of CIPK9 under Potassium-Deficient Conditions in Arabidopsis. Journal of Experimental Botany, 69, 4003-4015.
https://doi.org/10.1093/jxb/ery182

Jung, J.Y., Shin, R. and Schachtman, D.P. (2009) Ethylene Mediates Re-sponse and Tolerance to Potassium Deprivation in Arabidopsis. Plant Cell, 21, 607-621.
https://doi.org/10.1105/tpc.108.063099

Kim, M.J., Ruzicka, D., Shin, R. and Schachtman, D.P. (2012) The Arabidopsis AP2/ERF Transcription Factor RAP2.11 Modulates Plant Response to Low-Potassium Conditions. Mole-cular Plant, 5, 1042-1057.
https://doi.org/10.1093/mp/sss003

Cao, Y., Glass, A.D.M. and Crawford, N.M. (1993) Ammonium Inhibition of Arabidopsis Root Growth Can Be Reversed by Potassium and by Auxin Resistance Mutations aux1, axr1, and axr2. Plant Physiology, 102, 983-989.
https://doi.org/10.1104/pp.102.3.983

Li, J., Wu, W.H. and Wang, Y. (2017) Potassium Channel AKT1 Is Involved in the Auxin-Mediated Root Growth Inhibition in Arabidopsis Response to Low K+ Stress. Journal of Inte-grative Plant Biology, 59, 895-909.
https://doi.org/10.1111/jipb.12575

Shin, R., Burch, A.Y., Huppert, K., Tiwari, S.B., Murphy, A.S., Guilfoyle, T.J. and Schachtman, D.P. (2007) The Arabidopsis Transcription Factor MYB77 Modulates Auxin Signal Transduction. Plant Cell, 19, 2440-2453.
https://doi.org/10.1105/tpc.107.050963

Vicenteagullo, F., Rigas, S., Desbrosses, G., Dolan, L., Hatzopoulos, P. and Grabov, A. (2004) Potassium Carrier TRH1 Is Required for AuxinTransport in Arabidopsis Roots. The Plant Journal, 40, 523-535.
https://doi.org/10.1111/j.1365-313X.2004.02230.x

Dolan, L. (2013) Pointing PINs in the Right Directions: APotassium Transporter Is Required for the Polar Localization of AuxinEfflux Carriers. New Phytologist, 197, 1027-1028.
https://doi.org/10.1111/nph.12151

Rigas, S., Ditengou, F.A., Ljung, K., Daras, G., Tietz, O., Palme, K. and Hatzopoulos, P. (2013) Root Gravitropism and Root Hair Development Constitute Coupled Develop-mental Responses Regulated by Auxin Homeostasis in the Arabidopsis Root Apex. New Phytologist, 197, 1130-1141.
https://doi.org/10.1111/nph.12092

Osakabe, Y., Arinaga, N., Umezawa, T., Katsura, S., Nagamachi, K., Ta-naka, H., Ohiraki, H., Yamada, K., Seo, S.U. and Abo, M. (2013) Osmotic Stress Responses and Plant Growth Con-trolled by Potassium Transporters in Arabidopsis. The Plant Cell, 25, 609-624.
https://doi.org/10.1105/tpc.112.105700

Cellier, F., Conéjéro, G., Ricaud, L., Doan, T.L., Lepetit, M., Gosti, F. and Casse, F. (2004) Characterization of AtCHX17, a Member of the Cation/H+ Exchangers, CHX Family, from Arabidopsis Thaliana Suggests a Role in K+ Homeostasis. Plant Journal, 39, 834-846.
https://doi.org/10.1111/j.1365-313X.2004.02177.x

Li, G., Wu, Y., Liu, G., Xiao, X., Wang, P., Gao, T., Xu, M., Han, Q., Wang, Y. and Guo, T. (2017) Large-Scale Proteomics Combined with Transgenic Experiments Demon-strates an Important Role of Jasmonic Acid in Potassium Deficiency Response in Wheat and Rice. Molecular & Cellular Proteomics, 16, 1889-1905.
https://doi.org/10.1074/mcp.RA117.000032

Chen, Y., Ma, J., Miller, A.J., Luo, B., Wang, M., Zhu, Z. and Ouwerkerk, P.B.F. (2016) OsCHX14 Is Involved in the K+ Homeostasis in Rice (Oryza sativa) Flowers. Plant & Cell Physiology, 57, 1530-1543.
https://doi.org/10.1093/pcp/pcw088

Hu, B., Wang, W., Deng, K., Li, H., Zhang, Z., Zhang, L. and Chu, C. (2015) MicroRNA399 Is Involved in Multiple Nutrients Starvation Responses in Rice. Frontiers in Plant Science, 6, 188.
https://doi.org/10.3389/fpls.2015.00188

赵晓明. 番茄响应低钾胁迫关键基因的挖掘[D]: [博士学位论文]. 沈阳: 沈阳农业大学园艺学院, 2018.

刘杨. Sly-miR168α调控番茄钾养分吸收和利用的功能验证[D]: [硕士学位论文]. 沈阳: 沈阳农业大学园艺学院, 2018.

Li, L., Kim, B.G., Cheong, Y.H., Pandey, G.K. and Luan, S. (2006) A Ca2+ Signaling Pathway Regulates A K+ Channel for Low-K Response in Arabidopsis. Proceedings of the National Academy of Sciences of the United States of America, 103, 12625-12630.
https://doi.org/10.1073/pnas.0605129103

Min, J.K., Ciani, S. and Schachtman, D.P. (2010) A Peroxidase Contributes to ROS Production during Arabidopsis Root Response to Potassium Deficiency. Molecular Plant, 3, 420-427.
https://doi.org/10.1093/mp/ssp121

Shin, R., Schachtman, D.P. and Ryan, C.A. (2004) Hydrogen Peroxide Mediates Plant Root Cell Response to Nutrient Deprivation. Proceedings of the National Academy of Sciences of the United States of America, 101, 8827-8832.
https://doi.org/10.1073/pnas.0401707101

Yang, T., Zhang, S., Hu, Y., Wu, F., Hu, Q., Chen, G., Cai, J., Wu, T., Moran, N., Yu, L. and Xu, G. (2014) The Role of a Potassium Transporter OsHAK5 in Potassium Acquisition and Transport from Roots to Shoots in Rice at Low Potassium Supply Levels. Plant Physiology, 166, 945-959.
https://doi.org/10.1104/pp.114.246520

Zhang, H., Xiao, W., Yu, W., Yao, L., Li, L., Wei, J. and Li, R. (2018) Foxtail Millet SiHAK1 Excites Extreme High- Affinity K+ Uptake to Maintain K+ Homeostasis under Low K+ or Salt Stress. Plant Cell Reports, 37, 1533-1546.
https://doi.org/10.1007/s00299-018-2325-2

Cordones, M.N., Lara, A. and Rubio, F. (2019) Modulation of K+ Translocation by AKT1 and AtHAK5 in Arabidopsis Plants. Plant, Cell & Environment, 42, 2357-2371.
https://doi.org/10.1111/pce.13573

Zhao, S., Zhang, M.L., Ma, T.L. and Wang, Y. (2016) Phosphorylation of ARF2 Relieves Its Repression of Transcription of the K+ Transporter Gene HAK5 in Response to Low Potassium Stress. The Plant Cell, 28, 3005-3019.
https://doi.org/10.1105/tpc.16.00684

Hong, J.P., Takeshi, Y., Kondou, Y., Schachtman, D.P., Matsui, M. and Shin, R. (2013) Identification and Characterization of Transcription Factors Regulating Arabidopsis HAK5. Plant & Cell Physiology, 54, 1478-1490.
https://doi.org/10.1093/pcp/pct094

Li, H., Yu, M., Du, X.Q., Wang, Z.F., Wu, W.H., Quintero, F.J., Jin, X.H., Li, H.D. and Wang, Y. (2017) NRT1.5/ NPF7.3 Functions as a Proton-Coupled H+/K+ Antiporter for K+ Loading into the Xylem in Arabidopsis. Plant Cell, 29, 2016-2026.
https://doi.org/10.1105/tpc.16.00972

Du, X.Q., Wang, F.L., Li, H., Jing, S., Yu, M., Li, J., Wu, W.H., Kudla, J. and Wang, Y. (2019) The Transcription Factor MYB59 Regulates K+/NO3– Translocation in the Arabidopsis Response to Low K+ Stress. The Plant Cell, 31, 699-714.
https://doi.org/10.1105/tpc.18.00674

王二辉, 胡利芹, 薛飞洋, 李微微, 徐兆师, 李连诚, 周永斌. 谷子转录因子基因SiNAC45在拟南芥中对低钾及ABA的响应[J], 作物学报, 2015, 41(9): 1445-1453.

Lan, W.Z., Lee, S.C., Che, Y.F., Jiang, Y.Q. and Luan, S. (2011) Mechanistic Analysis of AKT1 Regulation by the CBL-CIPK-PP2CA Interactions. Molecular Plant, 4, 527-536.
https://doi.org/10.1093/mp/ssr031

Cherel, I., Michard, E., Platet, N., Mouline, K. and Thibaud, J.B. (2002) Physical and Functional Interaction of the Arabidopsis K+ Channel AKT2 and Phosphatase AtPP2CA. Plant Cell, 14, 1133-1146.
https://doi.org/10.1105/tpc.000943

Brauer, E.K., Ahsan, N., Dale, R., Kato, N., Coluccio, A.E., Kochian, L.V., Thelen, J.J. and Popescu, S.C. ( 2016) The Raf-Like Kinase ILK1 and the High Affinity K⁺ Transporter HAK5 Are Required for Innate Immunity and Abiotic Stress Response. Plant Physiology, 171, 1470-1484.
https://doi.org/10.1104/pp.16.00035

Simeunovic, A., Mair, A., Wurzinger, B. and Teige, M. (2016) Know Where Your Clients Are: Subcellular Localization and Targets of Calcium-Dependent Protein Kinases. Journal of Ex-perimental Botany, 67, 3855-3872.
https://doi.org/10.1093/jxb/erw157

Liu, L., Zheng, C., Kuang, B., Wei, L., Yan, L. and Wang, T. (2016) Receptor-Like Kinase RUPO Interacts with Potassium Transporters to Regulate Pollen Tube Growth and Integrity in Rice. PLoS Genetics, 12, e1006085.
https://doi.org/10.1371/journal.pgen.1006085

Zhao, L.N., Shen, L.K., Zhang, W.Z., Zhang, W., Wang, Y. and Wu, W.H. (2013) Ca2+-Dependent Protein Kinase11 and 24 Modulate the Activity of the Inward Rectifying K+ Channels in Arabidopsis Pollen Tubes. Plant Cell, 25, 649-661.
https://doi.org/10.1105/tpc.112.103184

Elsa, R., Claire, C., Frédéric, S., Karine, P. and Christian, B. (2014) CPK13, ANoncanonical Ca2+-Dependent Protein Kinase, Specifically Inhibits KAT2 and KAT1 Shaker K+ Channels and Reduces Stomatal Opening. Plant Physiology, 166, 314-326.
https://doi.org/10.1104/pp.114.240226

Corratgefaillie, C., Ronzier, E., Sanchez, F., Prado, K., Kim, J., Lanciano, S., Leonhardt, N., Lacombe, B. and Xiong, T.C. (2017) The Arabidopsis Guard Cell outward Potassium Channel GORK Is Regulated by CPK33. FEBS Letters, 591, 1982-1992.
https://doi.org/10.1002/1873-3468.12687

Jeanguenin, L., Alcon, C., Duby, G., Boeglin, M., Chérel, I., Gail-lard, I., Zimmermann, S., Sentenac, H. and Véry, A.A. (2011) AtKC1 Is a General Modulator of Arabidopsis Inward Shaker Channel Activity. Plant Journal, 67, 570-582.
https://doi.org/10.1111/j.1365-313X.2011.04617.x

Wang, Y., He, L., Li, H.D., Xu, J. and Wu, W.H. (2010) Potassium Channel α-Subunit AtKC1 Negatively Regulates AKT1-Mediated K+ Uptake in Arabidopsis Roots under Low-K+ Stress. Cell Research, 20, 826-837.
https://doi.org/10.1038/cr.2010.74

Wang, X.P., Chen, L.M., Liu, W.X., Shen, L.K., Wang, F.L., Zhou, Y., Zhang, Z., Wu, W.H. and Wang, Y. (2016) AtKC1 and CIPK23 Synergistically Modulate AKT1-Mediated Low-Potassium Stress Responses in Arabidopsis. Plant Physiology, 170, 2264-2277.
https://doi.org/10.1104/pp.15.01493

Zhang, B., Karnik, R., Wang, Y., Wallmeroth, N., Blatt, M.R. and Grefen, C. (2015) The Arabidopsis R-SNARE VAMP721 Interacts with KAT1 and KC1 K+ Channels to Moderate K+ Current at the Plasma Membrane. The Plant Cell, 27, 1697-1717.
https://doi.org/10.1105/tpc.15.00305

Zhang, A., Ren, H.M., Tan, Y.Q., Qi, G.N., Yao, F.Y., Wu, G.L., Yang, L.W., Hussain, J., Sun, S.J. and Wang, Y.F. (2016) S-Type Anion Channels SLAC1 and SLAH3 Function as Essential Negative Regulators of Inward K+ Channels and Stomatal Opening in Arabidopsis. Plant Cell, 28, 949-955.
https://doi.org/10.1105/tpc.15.01050