Abstract
AbstractPhosphorus is a macronutrient that regulates a wide range of physiological processes, including plant growth and development. The scarcity of bioavailable phosphate is often a constraint for plant growth in most agricultural ecosystems. Under phosphate limited conditions, plants increase phosphate acquisition or alter its distribution within tissues by activating different phosphate transporters and phosphate starvation-induced genes. Glutathione (GSH), on the other hand, is known to play a critical role in regulating iron and zinc homeostasis in Arabidopsis. However, how it regulates phosphate homeostasis under phosphate limited conditions remains unexplored. We found that the two GSH-deficient mutants,cad2-1, andpad2-1, were hypersensitive to phosphate starvation. Under phosphate-sufficient condition, the root phosphate content was lower in the mutants but significantly higher in the shoot over the Col-0 plants. The pattern was reversed under phosphate-deficient condition. Interestingly, among the different phosphate transporters analyzed, theAtPHT1;5was significantly down-regulated in the two GSH-deficient mutants. Treatment with exogenous GSH could alter phosphate accumulation in Col-0 and thepht1;5complementation lines but not in thepht1;5mutant. This observation confirmed the role of GSH in phosphate reallocation during phosphate starvation via theAtPHT1;5 transporter. Further, promoter analysis demonstrated that GSH regulates the transcription of theAtPHT1;5gene. The phosphate-responsive transcription factor (TF),AtWRKY75 was identified to interact with theAtPHT1;5promoter, and phosphate deficiency or GSH treatment enhanced its binding affinity. Together our investigation delineates that GSH regulates theAtPHT1;5 transporter via theAtWRKY75 TF to modulate phosphate distribution under altered phosphate conditions.Summary statementGlutathione regulates phosphate translocation in Arabidopsis under altered phosphate condition via transcriptional activation ofAtPHT1;5gene byAtWRKY75 transcription factor.
Publisher
Cold Spring Harbor Laboratory
Cited by
1 articles.
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