Kinase SnRK1.1 regulates nitrate channel SLAH3 engaged in nitrate-dependent alleviation of ammonium toxicity.
Kinase SnRK1.1 regulates nitrate channel SLAH3 engaged in nitrate-dependent alleviation of ammonium toxicity.
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激酶 SnRK1.1 调节硝酸盐通道 SLAH3，参与硝酸盐依赖性减轻铵毒性
DOI：
10.1093/plphys/kiab057
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发表时间：
2021-05-27
期刊：
影响因子：
7.4
通讯作者：
He K
中科院分区：
文献类型：
--
作者：
Sun D;Fang X;Xiao C;Ma Z;Huang X;Su J;Li J;Wang J;Wang S;Luan S;He K
Nitrate () and ammonium () are major inorganic nitrogen (N) supplies for plants, but as the sole or dominant N source causes growth inhibition in many plants, known as ammonium toxicity. Small amounts of can significantly mitigate ammonium toxicity, and the anion channel SLAC1 homolog 3 (SLAH3) is involved in this process, but the mechanistic detail of how SLAH3 regulates nitrate-dependent alleviation of ammonium toxicity is still largely unknown. In this study, we identified SnRK1.1, a central regulator involved in energy homeostasis, and various stress responses, as a SLAH3 interactor in Arabidopsis (Arabidopsis thaliana). Our results suggest that SNF1-related protein kinase 1 (SnRK1.1) functions as a negative regulator of SLAH3. Kinase assays indicate SnRK1.1 strongly phosphorylates the C-terminal of SLAH3 at the site S601. Under high-/low-pH condition, phospho-mimetic and phospho-dead mutations in SLAH3 S601 result in barely rescued phenotypes and fully complemented phenotypes in slah3. Furthermore, SnRK1.1 migrates from cytoplasm to nucleus under high-/low-pH conditions. The translocation of SnRK1.1 from cytosol to nucleus under high-ammonium stress releases the inhibition on SLAH3, which allows SLAH3-mediated efflux leading to alleviation of high-/low-pH stress. Our study reveals that the C-terminal phosphorylation also plays important role in SLAH3 regulation and provides additional insights into nitrate-dependent alleviation of ammonium toxicity in plants. Nitrate-dependent alleviation of ammonium toxicity involves negative regulation of a nitrate channel by a kinase.
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影响因子：
5.6
作者：
Crozet P;Margalha L;Confraria A;Rodrigues A;Martinho C;Adamo M;Elias CA;Baena-González E
通讯作者：
Baena-González E
DOI：
10.1073/pnas.0912021106
发表时间：
2009-12-15
影响因子：
11.1
作者：
Geiger, Dietmar;Scherzer, Soenke;Hedrich, Rainer
通讯作者：
Hedrich, Rainer
影响因子：
6.9
作者：
Koyama, H;Toda, T;Hara, T
通讯作者：
Hara, T
DOI：
10.1073/pnas.1116590109
发表时间：
2012-06-26
影响因子：
11.1
作者：
Brandt, Benjamin;Brodsky, Dennis E.;Schroeder, Julian I.
通讯作者：
Schroeder, Julian I.
影响因子：
7.3
作者：
Geiger, Dietmar;Maierhofer, Tobias;Hedrich, Rainer
通讯作者：
Hedrich, Rainer