中国农业大学国际著名学术期刊Plant Cell发表最新成果

　　

生物通报道：近日国际著名植物学杂志《Plant Cell》在线发表了中国农业大学题为“Phosphorylation of ARF2 Relieves its Repression of Transcription of the K+ transporter gene HAK5 in Response to Low Potassium Stress”的研究论文，这项研究结果表明，在拟南芥中ARF2参与K+吸收的调控。它的功能是作为一个转录抑制因子，并调节HAK5的转录，响应低的K+胁迫。中国农业大学生物学院植物生理学与生物化学国家重点实验室的副教授王毅，是本文通讯作者。

钾（K +）在植物生长发育中起着至关重要的作用。在自然环境中，土壤中钾的有效性相对较低且波动性较大。K +转运蛋白基因的转录调控，是植物响应钾缺乏症的最重要的机制之一。在这项研究中，研究人员证实，在拟南芥中，转录因子ARF2（Auxin Response Factor 2）调节着K+转运基因HAK5（High Affinity K+ transporter 5）的表达。在低钾含量的培养基上，ARF2突变体植株表现出类似于HAK5过表达品系的抗性表型，其主根长度比野生型植株的长。

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在这些植物中，高亲和力的K +吸收显著增加。ARF2过表达品系和Hak5突变体，都对低钾胁迫非常的敏感。在arf2突变体中的Hak5中断，可消除arf2的低钾抗性表型。作为一个转录抑制因子，ARF2可直接结合到HAK5启动子，并在K+充分的条件下抑制Hak5表达。在低钾处理后，ARF2可被磷酸化，这会消除其与HAK5启动子的DNA结合活性，并解除对HAK5转录的抑制。因此，在K+缺乏的条件下，HAK5转录本可以被诱导，HAK5介导的高亲和力K +吸收得以增强。这些结果表明，ARF2在拟南芥响应外部钾供应中发挥重要的作用，并相应地调节HAK5转录。

在2014年8月，王毅带领的研究小组在《Plant Cell》发表一项研究，分析了Os-CBL1和Os-CIPK23对其的调控。作为一个内向钾离子通道，Os-AKT1能进行K+吸收，并解救拟南芥akt1突变体植株的低钾敏感表型。水稻Os-akt1突变体植株表现出K+吸收下降，和明显的低钾敏感表型。破坏Os-AKT1，可显著降低K+含量，这会导致植物生长和发育的抑制作用。类似于拟南芥中的AKT1调控，Os-CBL1和Os-CIPK23被确定为水稻Os-AKT1的上游调节因子。相关阅读：中国农大《Plant Cell》阐释水稻K+吸收机制。

（生物通：王英）

生物通推荐原文摘要：
Phosphorylation of ARF2 Relieves its Repression of Transcription of the K+ transporter gene HAK5 in Response to Low Potassium Stress
Abstract：Potassium (K+) plays crucial roles in plant growth and development. In natural environments, K+ availability in soils is relatively low and fluctuating. Transcriptional regulation of K+ transporter genes is one of the most important mechanisms in the plant's response to K+ deficiency. In this study, we demonstrated that the transcription factor ARF2 (Auxin Response Factor 2) modulates the expression of the K+ transporter gene HAK5 (High Affinity K+ transporter 5) in Arabidopsis thaliana. The arf2 mutant plants showed a tolerant phenotype similar to the HAK5-overexpressing lines on low-K+ medium, whose primary root lengths were longer than those of wild-type plants. High-affinity K+ uptake was significantly increased in these plants. ARF2-overexpressing lines and the hak5 mutant were both sensitive to low-K+ stress. Disruption of HAK5 in the arf2 mutant abolished the low-K+-tolerant phenotype of arf2. As a transcriptional repressor, ARF2 directly bound to the HAK5 promoter and repressed HAK5 expression under K+ sufficient conditions. ARF2 can be phosphorylated after low-K+ treatment, which abolished its DNA-binding activity to the HAK5 promoter and relieved the inhibition on HAK5 transcription. Therefore, HAK5 transcript could be induced, and HAK5-mediated high-affinity K+ uptake was enhanced under K+ deficient conditions. The presented results demonstrate that ARF2 plays important roles in the response to external K+ supply in Arabidopsis and regulates HAK5 transcription accordingly.