State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China; Department of Biology, Duke University, Durham, NC 27008, USA.
State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China; Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA.
J Genet Genomics. 2023 Jul;50(7):473-485. doi: 10.1016/j.jgg.2023.05.001. Epub 2023 May 13.
The phytohormone auxin plays crucial roles in nearly every aspect of plant growth and development. Auxin signaling is activated through the phytohormone-induced proteasomal degradation of the Auxin/INDOLE-3-ACETIC ACID (Aux/IAA) family of transcriptional repressors. Notably, many auxin-modulated physiological processes are also regulated by nitric oxide (NO) that executes its biological effects predominantly through protein S-nitrosylation at specific cysteine residues. However, little is known about the molecular mechanisms in regulating the interactive NO and auxin networks. Here, we show that NO represses auxin signaling by inhibiting IAA17 protein degradation. NO induces the S-nitrosylation of Cys-70 located in the intrinsically disordered region of IAA17, which inhibits the TIR1-IAA17 interaction and consequently the proteasomal degradation of IAA17. The accumulation of a higher level of IAA17 attenuates auxin response. Moreover, an IAA17 nitrosomimetic mutation renders the accumulation of a higher level of the mutated protein, thereby causing partial resistance to auxin and defective lateral root development. Taken together, these results suggest that S-nitrosylation of IAA17 at Cys-70 inhibits its interaction with TIR1, thereby negatively regulating auxin signaling. This study provides unique molecular insights into the redox-based auxin signaling in regulating plant growth and development.
植物激素生长素在植物生长和发育的几乎所有方面都起着至关重要的作用。生长素信号通过植物激素诱导的转录抑制因子Aux/IAA 家族的蛋白体降解来激活。值得注意的是，许多生长素调节的生理过程也受一氧化氮（NO）的调节，NO 主要通过特定半胱氨酸残基上的蛋白质 S-亚硝基化来执行其生物学效应。然而，关于调节相互作用的 NO 和生长素网络的分子机制知之甚少。在这里，我们表明 NO 通过抑制 IAA17 蛋白降解来抑制生长素信号。NO 诱导位于 IAA17 无规卷曲区域的 Cys-70 的 S-亚硝基化，从而抑制 TIR1-IAA17 相互作用，进而抑制 IAA17 的蛋白体降解。IAA17 水平的升高会减弱生长素的反应。此外，IAA17 的一个硝酰化模拟突变导致突变蛋白的积累水平升高，从而导致对生长素的部分抗性和侧根发育缺陷。总之，这些结果表明，IAA17 在 Cys-70 的 S-亚硝基化抑制了它与 TIR1 的相互作用，从而负调控生长素信号。这项研究为基于氧化还原的生长素信号在调节植物生长和发育中的作用提供了独特的分子见解。
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