Remans Tony, Nacry Philippe, Pervent Marjorie, Filleur Sophie, Diatloff Eugene, Mounier Emmanuelle, Tillard Pascal, Forde Brian G, Gojon Alain
Biochimie et Physiologie Moléculaire des Plantes, Institut National de la Recherche Agronomique, Centre National de la Recherche Scientifique, UM2, et AgroM, Place Viala, F-34060 Montpellier, France.
Proc Natl Acad Sci U S A. 2006 Dec 12;103(50):19206-11. doi: 10.1073/pnas.0605275103. Epub 2006 Dec 5.
Localized proliferation of lateral roots in NO(3)(-)-rich patches is a striking example of the nutrient-induced plasticity of root development. In Arabidopsis, NO(3)(-) stimulation of lateral root elongation is apparently under the control of a NO(3)(-)-signaling pathway involving the ANR1 transcription factor. ANR1 is thought to transduce the NO(3)(-) signal internally, but the upstream NO(3)(-) sensing system is unknown. Here, we show that mutants of the NRT1.1 nitrate transporter display a strongly decreased root colonization of NO(3)(-)-rich patches, resulting from reduced lateral root elongation. This phenotype is not due to lower specific NO(3)(-) uptake activity in the mutants and is not suppressed when the NO(3)(-)-rich patch is supplemented with an alternative N source but is associated with dramatically decreased ANR1 expression. These results show that NRT1.1 promotes localized root proliferation independently of any nutritional effect and indicate a role in the ANR1-dependent NO(3)(-) signaling pathway, either as a NO(3)(-) sensor or as a facilitator of NO(3)(-) influx into NO(3)(-)-sensing cells. Consistent with this model, the NRT1.1 and ANR1 promoters both directed reporter gene expression in root primordia and root tips. The inability of NRT1.1-deficient mutants to promote increased lateral root proliferation in the NO(3)(-)-rich zone impairs the efficient acquisition of NO(3)(-) and leads to slower plant growth. We conclude that NRT1.1, which is localized at the forefront of soil exploration by the roots, is a key component of the NO(3)(-)-sensing system that enables the plant to detect and exploit NO(3)(-)-rich soil patches.
在富含硝酸根(NO₃⁻)的区域侧根的局部增殖是营养诱导根系发育可塑性的一个显著例子。在拟南芥中,NO₃⁻对侧根伸长的刺激显然受涉及ANR1转录因子的NO₃⁻信号通路的控制。ANR1被认为在内部转导NO₃⁻信号,但上游的NO₃⁻感知系统尚不清楚。在这里,我们表明NRT1.1硝酸盐转运蛋白的突变体在富含NO₃⁻的区域根系定殖能力大幅下降,这是由于侧根伸长减少所致。这种表型并非由于突变体中较低的特定NO₃⁻吸收活性,并且当富含NO₃⁻的区域补充替代氮源时也不会被抑制,而是与ANR1表达的显著降低有关。这些结果表明,NRT1.1独立于任何营养效应促进局部根系增殖,并表明其在依赖ANR1的NO₃⁻信号通路中发挥作用,要么作为NO₃⁻传感器,要么作为促进NO₃⁻流入NO₃⁻感知细胞的因子。与该模型一致,NRT1.1和ANR1启动子都在根原基和根尖中指导报告基因的表达。NRT1.1缺陷型突变体无法在富含NO₃⁻的区域促进侧根增殖增加,这损害了对NO₃⁻的有效获取并导致植物生长缓慢。我们得出结论,位于根系土壤探索前沿的NRT1.1是NO₃⁻感知系统的关键组成部分,使植物能够检测和利用富含NO₃⁻的土壤区域。