z-logo
Premium
Abscisic acid signaling negatively regulates nitrate uptake via phosphorylation of NRT1.1 by SnRK2s in Arabidopsis
Author(s) -
Su Hang,
Wang Tian,
Ju Chuanfeng,
Deng Jinping,
Zhang Tianqi,
Li Mengjiao,
Tian Hui,
Wang Cun
Publication year - 2021
Publication title -
journal of integrative plant biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.734
H-Index - 83
eISSN - 1744-7909
pISSN - 1672-9072
DOI - 10.1111/jipb.13057
Subject(s) - abscisic acid , arabidopsis thaliana , arabidopsis , phosphorylation , nitrate , mutant , biochemistry , biology , kinase , microbiology and biotechnology , chemistry , gene , ecology
Nitrogen (N) is a limiting nutrient for plant growth and productivity. The phytohormone abscisic acid (ABA) has been suggested to play a vital role in nitrate uptake in fluctuating N environments. However, the molecular mechanisms underlying the involvement of ABA in N deficiency responses are largely unknown. In this study, we demonstrated that ABA signaling components, particularly the three subclass III SUCROSE NON‐FERMENTING1 (SNF1)‐RELATED PROTEIN KINASE 2S (SnRK2) proteins, function in root foraging and uptake of nitrate under N deficiency in Arabidopsis thaliana . The snrk2.2snrk2.3snrk2.6 triple mutant grew a longer primary root and had a higher rate of nitrate influx and accumulation compared with wild‐type plants under nitrate deficiency. Strikingly, SnRK2.2/2.3/2.6 proteins interacted with and phosphorylated the nitrate transceptor NITRATE TRANSPORTER1.1 (NRT1.1) in vitro and in vivo . The phosphorylation of NRT1.1 by SnRK2s resulted in a significant decrease of nitrate uptake and impairment of root growth. Moreover, we identified NRT1.1 Ser585 as a previously unknown functional site: the phosphomimetic NRT1.1 S585D was impaired in both low‐ and high‐affinity transport activities. Taken together, our findings provide new insight into how plants fine‐tune growth via ABA signaling under N deficiency.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here