Castillo Mari-Cruz, Lozano-Juste Jorge, González-Guzmán Miguel, Rodriguez Lesia, Rodriguez Pedro L, León José
Instituto de Biología Molecular y Celular de Plantas (Consejo Superior de Investigaciones Científicas-Universidad Politécnica de Valencia), CPI Edificio 8E, Avda. Ingeniero Fausto Elio s/n, 46022 Valencia, Spain.
Sci Signal. 2015 Sep 1;8(392):ra89. doi: 10.1126/scisignal.aaa7981.
Abscisic acid (ABA) is a phytohormone that inhibits growth and enhances adaptation to stress in plants. ABA perception and signaling rely on its binding to receptors of the pyrabactin resistance1/PYR1-like/regulatory components of ABA receptors (PYR/PYL/RCAR) family, the subsequent inhibition of clade A type 2C protein phosphatases (PP2Cs), and the phosphorylation of ion channels and transcription factors by protein kinases of the SnRK2 family. Nitric oxide (NO) may inhibit ABA signaling because NO-deficient plants are hypersensitive to ABA. Regulation by NO often involves posttranslational modification of proteins. Mass spectrometry analysis of ABA receptors expressed in plants and recombinant receptors modified in vitro revealed that the receptors were nitrated at tyrosine residues and S-nitrosylated at cysteine residues. In an in vitro ABA-induced, PP2C inhibition assay, tyrosine nitration reduced receptor activity, whereas S-nitrosylated receptors were fully capable of ABA-induced inhibition of the phosphatase. PYR/PYL/RCAR proteins with nitrated tyrosine, which is an irreversible covalent modification, were polyubiquitylated and underwent proteasome-mediated degradation. We propose that tyrosine nitration, which requires NO and superoxide anions, is a rapid mechanism by which NO limits ABA signaling under conditions in which NO and reactive oxygen species are both produced.
脱落酸（ABA）是一种植物激素，它能抑制植物生长并增强植物对胁迫的适应性。ABA的感知和信号传导依赖于其与脱落酸受体（PYR/PYL/RCAR）家族的吡唑啉酮抗性1/类PYR1/调节成分受体的结合，随后抑制A类2C型蛋白磷酸酶（PP2C），以及由SnRK2家族蛋白激酶对离子通道和转录因子进行磷酸化。一氧化氮（NO）可能抑制ABA信号传导，因为缺乏NO的植物对ABA高度敏感。NO的调节通常涉及蛋白质的翻译后修饰。对植物中表达的ABA受体和体外修饰的重组受体进行质谱分析发现，这些受体在酪氨酸残基处发生硝化，在半胱氨酸残基处发生S-亚硝基化。在体外ABA诱导的PP2C抑制试验中，酪氨酸硝化降低了受体活性，而S-亚硝基化受体完全能够被ABA诱导抑制磷酸酶。具有硝化酪氨酸的PYR/PYL/RCAR蛋白是一种不可逆的共价修饰，被多聚泛素化并经历蛋白酶体介导的降解。我们提出，需要NO和超氧阴离子的酪氨酸硝化是一种快速机制，通过该机制，在同时产生NO和活性氧的条件下，NO限制ABA信号传导。
