Genetic and transcriptomic dissection of nitrate-independent function of Arabidopsis NRT1.1/NPF6.3/CHL1 under high ammonium condition

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Genetic and transcriptomic dissection of nitrate-independent function of Arabidopsis NRT1.1/NPF6.3/CHL1 under high ammonium condition

Authors

Hachiya, T.; Makita, N.; Bach, L.; Gojon, A.; Nakagawa, T.; Sakakibara, H.

Abstract

The Arabidopsis nitrate transceptor NRT1.1/NPF6.3/CHL1 regulates physiological responses to nitrate. Several studies have reported that Arabidopsis lacking NRT1.1 shows enhanced shoot growth, even without nitrate, suggesting a nitrate-independent function for NRT1.1. To further investigate this nitrate-independent function and its impact on ammonium tolerance, we conducted genetic analysis, tissue-specific expression analysis, and transcriptome analysis using various NRT1.1-related lines. Transgenic plants expressing either nonphosphomimic or phosphomimic mutants of NRT1.1 exhibited similar ammonium tolerance to the wild-type. The chl1-9 mutant, in which NRT1.1 with the P492L substitution is localized intracellularly rather than at the plasma membrane and fails to transport nitrate, showed significantly improved ammonium tolerance. Our confocal observations revealed that the NRT1.1-GFP loop signal was detected in the plasma membrane of various tissues, including cotyledon pavement cells, hypocotyl epidermal cells, mesophyll cells, and epidermis and cortex near root tips. In early seedlings, the absence of functional NRT1.1 altered the expression of genes associated with aliphatic glucosinolate biosynthesis, ethylene signaling, and low pH stress. Genes predicted to encode products localized to the extracellular space were enriched among those differentially expressed due to NRT1.1 deficiency. Collectively, our data suggest that in the absence of nitrate, plasma membrane-targeted NRT1.1 reduces ammonium tolerance irrespective of its phosphorylation state by altering gene expression associated with stress and senescence.

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