Emerging Players in the Nitrate Signaling Pathway

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Emerging Players in the Nitrate Signaling Pathway Grace Armijo, Rodrigo A. Gutiérrez  Molecular Plant  Volume 10, Issue 8, Pages 1019-1022 (August 2017) DOI: 10.1016/j.molp.2017.07.006 Copyright © 2017 The Author Terms and Conditions

Figure 1 An Updated Model of the Nitrate Signaling Pathway. The proposed NRT1.1 transceptor activates signal transduction cascades that regulate responses to nitrate. NRT1.1 displays either high or low affinity for nitrate depending on phosphorylation status. The CIPK23-CBL9 complex plays a role in the dual-affinity transition changes of NRT1.1, while ABI2 and CBL1 that interacts with dephosphorylated CIPK23 were identified as additional components of this regulation process. Nitrate perception induces a rapid increase in cytoplasmic Ca2+ levels downstream of NRT1.1 in a process that requires PLC activity. A Ca2+/PLC-independent signaling pathway may also exist with target genes such as AFB3 and NAC4. One of the direct consequences of increase in Ca2+ is the change in protein phosphorylation status, controlling the activity of key components of the nitrate signaling pathway. CPK10, CPK30 and CPK32 function as master regulators of primary nitrate responses, connecting the influx of calcium and phosphorylation of target proteins. Activation of CPKs could be related to an NRT1.1-dependent pathway. However, it is also possible that additional nitrate sensors and an NRT1.1-independent pathway could contribute to calcium influx and other signaling events. CPK signaling phosphorylates NLP transcription factors, specifically NLP7, which interacts in the nucleus with CPK10 in the presence of nitrate. In addition to NLPs, others transcription factors such as TCP20 also play critical roles in nitrate-induced transcriptional changes and systemic signaling, while TGA1 and TGA4 regulate genes involved in primary nitrate response, transport, and metabolic and developmental functions. Molecular Plant 2017 10, 1019-1022DOI: (10.1016/j.molp.2017.07.006) Copyright © 2017 The Author Terms and Conditions