A NIGT1-centred transcriptional cascade regulates nitrate signalling and incorporates phosphorus starvation signals in Arabidopsis

Yoshie Maeda, Mineko Konishi, Takatoshi Kiba, Yasuhito Sakuraba, Naoya Sawaki, Tomohiro Kurai, Yoshiaki Ueda, Hitoshi Sakakibara and Shuichi Yanagisawa ()
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Yoshie Maeda: The University of Tokyo
Mineko Konishi: The University of Tokyo
Takatoshi Kiba: RIKEN Center for Sustainable Resource Science
Yasuhito Sakuraba: The University of Tokyo
Naoya Sawaki: The University of Tokyo
Tomohiro Kurai: The University of Tokyo
Yoshiaki Ueda: The University of Tokyo
Hitoshi Sakakibara: RIKEN Center for Sustainable Resource Science
Shuichi Yanagisawa: The University of Tokyo

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Nitrate is a nutrient signal that triggers complex regulation of transcriptional networks to modulate nutrient-dependent growth and development in plants. This includes time- and nitrate concentration-dependent regulation of nitrate-related gene expression. However, the underlying mechanisms remain poorly understood. Here we identify NIGT1 transcriptional repressors as negative regulators of the Arabidopsis NRT2.1 nitrate transporter gene, and show antagonistic regulation by NLP primary transcription factors for nitrate signalling and the NLP-NIGT1 transcriptional cascade-mediated repression. This antagonistic regulation provides a resolution to the complexity of nitrate-induced transcriptional regulations. Genome-wide analysis reveals that this mechanism is applicable to NRT2.1 and other genes involved in nitrate assimilation, hormone biosynthesis and transcription. Furthermore, the PHR1 master regulator of the phosphorus-starvation response also directly promotes expression of NIGT1 family genes, leading to reductions in nitrate uptake. NIGT1 repressors thus act in two transcriptional cascades, forming a direct link between phosphorus and nitrogen nutritional regulation.

Date: 2018
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03832-6

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DOI: 10.1038/s41467-018-03832-6

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