Regulatory functions of cellular energy sensor SnRK1 for nitrate signalling through NLP7 repression
Regulatory functions of cellular energy sensor SnRK1 for nitrate signalling through NLP7 repression
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DOI：
10.1038/s41477-022-01236-5
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发表时间：
2022-09-01
期刊：
影响因子：
18
通讯作者：
Bai, Ming-Yi
中科院分区：
文献类型：
--
作者：
Wang, Honglei;Han, Chao;Bai, Ming-Yi
碳和氮的协调代谢对植物的最佳生长和发育至关重要。硝酸盐是植物适应环境变化的重要分子信号，但在缺碳条件下硝酸盐如何调控植物生长尚不清楚。在这里，我们证明了进化上保守的能量传感器SnRK1负调控硝酸盐信号通路。硝酸盐促进植物生长和下游基因表达，但当植物生长在缺碳条件下时，这种作用受到抑制。SnRK1α催化亚基KIN10的突变部分抑制了缺碳对硝酸盐介导的植物生长的抑制作用。KIN10磷酸化NLP7，促进NLP7的胞质定位和降解。NLP7是硝酸盐信号通路的主要调节因子。此外，硝酸盐耗竭导致KIN10的积累，而硝酸盐处理促进KIN10的降解。这种KIN10介导的NLP7调控允许碳和硝酸盐的利用来控制最佳的硝酸盐信号，并确保植物中碳和氮代谢的协调。进化上保守的能量传感器SnRK1与NLP7相互作用并磷酸化NLP7，促进其细胞质定位和降解，从而抑制硝酸盐信号转导。
The coordinated metabolism of carbon and nitrogen is essential for optimal plant growth and development. Nitrate is an important molecular signal for plant adaptation to a changing environment, but how nitrate regulates plant growth under carbon deficiency conditions remains unclear. Here we show that the evolutionarily conserved energy sensor SnRK1 negatively regulates the nitrate signalling pathway. Nitrate promoted plant growth and downstream gene expression, but such effects were repressed when plants were grown under carbon deficiency conditions. Mutation of KIN10, the alpha-catalytic subunit of SnRK1, partially suppressed the inhibitory effects of carbon deficiency on nitrate-mediated plant growth. KIN10 phosphorylated NLP7, the master regulator of the nitrate signalling pathway, to promote its cytoplasmic localization and degradation. Furthermore, nitrate depletion induced KIN10 accumulation, whereas nitrate treatment promoted KIN10 degradation. Such KIN10-mediated NLP7 regulation allows carbon and nitrate availability to control optimal nitrate signalling and ensures the coordination of carbon and nitrogen metabolism in plants.The evolutionarily conserved energy sensor SnRK1 interacts with and phosphorylates NLP7 to promote its cytoplasmic localization and degradation, thereby inhibiting nitrate signalling.