Salt-Sensitive Signaling Networks in the Mediation of K+/Na+ Homeostasis Gene Expression in Glycyrrhiza uralensis Roots

Sodium–hydrogen antiporter Glycyrrhiza uralensis
DOI: 10.3389/fpls.2017.01403 Publication Date: 2017-08-14T05:13:49Z
ABSTRACT
We investigated the effects of salt-sensitive signaling molecules on ionic fluxes and gene expression related to K+/Na+ homeostasis in a perennial herb, Glycyrrhiza uralensis, during short-term NaCl stress (100 mM, 24 h). Salt treatment caused more pronounced Na+ accumulation root cells than leaf cells. ions were mostly compartmentalized vacuoles. Roots exposed showed increased levels extracellular ATP (eATP), cytosolic Ca2+, H2O2, NO. Steady-state flux recordings revealed that these enhanced NaCl-responsive efflux, due activated Na+/H+ antiport system plasma membrane (PM). Moreover, salt-elicited K+ which was mediated by depolarization-activated cation channels, reduced with addition NO, eATP. The salt-adaptive (Na+ extrusion maintenance) pharmacological agents, including LaCl3 (a PM Ca2+ channel inhibitor), DMTU reactive oxygen species scavenger), cPTIO (an NO or PPADS antagonist animal purine P2 receptors). RT-qPCR data activation salinized roots most likely resulted from upregulation two genes, GuSOS1 GuAHA, encoded antiporter, salt overly sensitive 1 (SOS1) H+-ATPase, respectively. Clear interactions occurred between agonists accelerate transcription salt-responsive pathway genes G. uralensis roots. For example, eATP promoted GuSOS3 (salt 3) and/or GuCIPK (CBL-interacting protein kinase) activate predominant Ca2+-SOS liquorice eATP, novel player response GuSOS3, GuCIPK, GuRbohD (respiratory burst oxidase homolog D), GuNIR (nitrate reductase), GuMAPK3, GuMAPK6 (the mitogen-activated kinases 3 6). GuMAPK3 H2O2 NaCl-stressed Our results indicated triggered downstream components interacted maintain homeostasis. propose multiple network regulated
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