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(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)^(+)/Iow-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.展开更多
基金supported by the National Natural Science Foundation of China(31870235,32170280)the 111 Project(B16022)the Fundamental Research Funds for the Central Universities(lzujbky-2019-kb05,lzujbky-2020-kb05,lzujbky-2021-it22)。
文摘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)^(+)/Iow-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.
