Discovery of nitrate–CPK–NLP signalling in central nutrient–growth networks

Kun-hsiang Liu (), Yajie Niu, Mineko Konishi, Yue Wu, Hao Du, Hoo Sun Chung, Lei Li, Marie Boudsocq, Matthew McCormack, Shugo Maekawa, Tetsuya Ishida, Chao Zhang, Kevan Shokat, Shuichi Yanagisawa () and Jen Sheen ()
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Kun-hsiang Liu: Massachusetts General Hospital, Harvard Medical School
Yajie Niu: Massachusetts General Hospital, Harvard Medical School
Mineko Konishi: Biotechnology Research Center, The University of Tokyo
Yue Wu: Massachusetts General Hospital, Harvard Medical School
Hao Du: Massachusetts General Hospital, Harvard Medical School
Hoo Sun Chung: Massachusetts General Hospital, Harvard Medical School
Lei Li: Massachusetts General Hospital, Harvard Medical School
Marie Boudsocq: Massachusetts General Hospital, Harvard Medical School
Matthew McCormack: Massachusetts General Hospital, Harvard Medical School
Shugo Maekawa: Biotechnology Research Center, The University of Tokyo
Tetsuya Ishida: Biotechnology Research Center, The University of Tokyo
Chao Zhang: UCSF
Kevan Shokat: UCSF
Shuichi Yanagisawa: Biotechnology Research Center, The University of Tokyo
Jen Sheen: Massachusetts General Hospital, Harvard Medical School

Nature, 2017, vol. 545, issue 7654, 311-316

Abstract: Abstract Nutrient signalling integrates and coordinates gene expression, metabolism and growth. However, its primary molecular mechanisms remain incompletely understood in plants and animals. Here we report unique Ca2+ signalling triggered by nitrate with live imaging of an ultrasensitive biosensor in Arabidopsis leaves and roots. A nitrate-sensitized and targeted functional genomic screen identifies subgroup III Ca2+-sensor protein kinases (CPKs) as master regulators that orchestrate primary nitrate responses. A chemical switch with the engineered mutant CPK10(M141G) circumvents embryo lethality and enables conditional analyses of cpk10 cpk30 cpk32 triple mutants to define comprehensive nitrate-associated regulatory and developmental programs. Nitrate-coupled CPK signalling phosphorylates conserved NIN-LIKE PROTEIN (NLP) transcription factors to specify the reprogramming of gene sets for downstream transcription factors, transporters, nitrogen assimilation, carbon/nitrogen metabolism, redox, signalling, hormones and proliferation. Conditional cpk10 cpk30 cpk32 and nlp7 mutants similarly impair nitrate-stimulated system-wide shoot growth and root establishment. The nutrient-coupled Ca2+ signalling network integrates transcriptome and cellular metabolism with shoot–root coordination and developmental plasticity in shaping organ biomass and architecture.

Date: 2017
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DOI: 10.1038/nature22077

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