Nitrate transporter NRT1.1 and anion channel SLAH3 form a functional unit to regulate nitrate-dependent alleviation of ammonium toxicity
Nitrate transporter NRT1.1 and anion channel SLAH3 form a functional unit to regulate nitrate-dependent alleviation of ammonium toxicity
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硝酸盐转运蛋白 NRT1.1 和阴离子通道 SLAH3 形成功能单元，调节硝酸盐依赖性缓解铵毒性
DOI：
10.1111/jipb.13239
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发表时间：
2022
影响因子：
11.4
通讯作者：
He Kai
中科院分区：
文献类型：
--
作者：
Xiao Chengbin;Sun Doudou;Liu Beibei;Fang Xianming;Li Pengcheng;Jiang Yao;He Mingming;Li Jia;Luan Sheng;He Kai
铵(NH_4~+)和硝酸盐(NO_3~-)是植物主要的无机氮(N)源。当NH_4~+作为唯一或主导氮源时,常引起植物根部抑制和茎部失绿,称为铵毒性。NO_3~-通常不产生毒性,即使在低浓度下也能减轻铵毒性,称为硝酸盐依赖性铵毒性减轻。 NO_3~-流出通道SLAH3参与了这一过程。然而，其他成分是否有助于NO_3~-介导的NH_4~+解毒尚不清楚。之前，NO_3~-转运蛋白NRT1.1的突变被证明会导致对高浓度NH_4~+的抵抗力增强。而在本研究中，我们发现当高NH_4~+培养基中添加低浓度的NH_4~+时， NO_3~-,nrt1.1突变体反而表现出超敏感表型。此外,NRT1.1突变导致高NH_4~+/低NO_3~-条件下培养基酸化增强,表明NRT1.1通过促进H~+吸收来调节铵毒性。此外,NRT1.1与SLAH3相互作用形成转运通道复合物。有趣的是,SLAH3似乎NRT1.1影响NO_3~-内流，而NRT1.1影响NO_3~-外流，表明NRT1.1和SLAH3在蛋白质和/或基因表达水平上相互调节。因此，我们的研究揭示了NRT1.1和SLAH3形成一个功能单元，通过调节NO_3~-转运和平衡根际酸化来调节硝酸盐依赖性铵毒性的缓解。
Ammonium (NH_4~+) and nitrate (NO_3~-) are major inorganic nitrogen (N) sources for plants.When serving as the sole or dominant N supply,NH_4~+ often causes root inhibition and shoot chlorosis in plants,known as ammonium toxicity.NO_3~-usually causes no toxicity and can mitigate ammonium toxicity even at low concentrations,referred to as nitrate-dependent alleviation of ammonium toxicity.Our previous studies indicated a NO_3~-efflux channel SLAH3 is involved in this process.However,whether additional components contribute to NO_3~--mediated NH_4~+ detoxification is unknown.Previously,mutations in NO_3~- transporter NRT1.1 were shown to cause enhanced resistance to high concentrations of NH_4~+.Whereas,in this study,we found when the high-NH_4~+ medium was supplemented with low concentrations of NO_3~-,nrt1.1 mutant plants showed hyper-sensitive phenotype instead.Furthermore,mutation in NRT1.1 caused enhanced medium acidification under high-NH_4~+/low-NO_3~- condition,suggesting NRT1.1 regulates ammonium toxicity by facilitating H~+uptake.Moreover,NRT1.1 was shown to interact with SLAH3 to form a transporter-channel complex.Interestingly,SLAH3 appeared to affect NO_3~- influx while NRT1.1 influenced NO_3~- efflux,suggesting NRT1.1 and SLAH3 regulate each other at protein and/or gene expression levels.Our study thus revealed NRT1.1 and SLAH3 form a functional unit to regulate nitrate-dependent alleviation of ammonium toxicity through regulating NO_3~- transport and balancing rhizosphere acidification.