Regulatory functions of cellular energy sensor SnRK1 for nitrate signalling through NLP7 repression

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.

Automated summary

This study reveals that SnRK1 negatively regulates the nitrate signalling pathway, inhibiting the effects of nitrate on plant growth under carbon deficiency conditions. KIN10 phosphorylates NLP7 to affect the regulatory activity of the nitrate signalling pathway.