Fundación Instituto Leloir, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Investigaciones Bioquímicas de Buenos Aires, Buenos Aires 1405, Argentina.
Departamento de Fisiología, Biología Molecular y Celular and Consejo de Investigaciones Científicas y Técnicas, Facultad de Ciencias Exactas y Naturales, Instituto de Fisiología, Biología Molecular y Neurociencias, Universidad de Buenos Aires, Buenos Aires 1428, Argentina.
Proc Natl Acad Sci U S A. 2024 Oct 15;121(42):e2320187121. doi: 10.1073/pnas.2320187121. Epub 2024 Oct 9.
Canopy shade enhances the activity of PHYTOCHROME INTERACTING FACTORs (PIFs) to boost auxin synthesis in the cotyledons. Auxin, together with local PIFs and their positive regulator CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1), promotes hypocotyl growth to facilitate access to light. Whether shade alters the cellular redox status thereby affecting growth responses, remains unexplored. Here, we show that, under shade, high auxin levels increased reactive oxygen species and nitric oxide accumulation in the hypocotyl of This nitroxidative environment favored the promotion of hypocotyl growth by COP1 under shade. We demonstrate that COP1 is S-nitrosylated, particularly under shade. Impairing this redox regulation enhanced COP1 degradation by the proteasome and diminished the capacity of COP1 to interact with target proteins and to promote hypocotyl growth. Disabling this regulation also generated transversal asymmetries in hypocotyl growth, indicating poor coordination among different cells, which resulted in random hypocotyl bending and predictably low ability to compete with neighbors. These findings highlight the significance of redox signaling in the control of diffuse growth during shade avoidance.
冠层遮荫增强了 PHYTOCHROME INTERACTING FACTORs（PIFs）的活性，从而促进子叶中生长素的合成。生长素与局部的 PIFs 及其正调控因子 CONSTITUTIVELY PHOTOMORPHOGENIC 1（COP1）一起促进下胚轴生长，以利于获得光照。然而，遮荫是否会改变细胞的氧化还原状态从而影响生长反应，这一点仍未得到探索。在这里，我们表明，在遮荫下，高生长素水平会增加下胚轴中活性氧和一氧化氮的积累。这种氮氧化环境有利于 COP1 在遮荫下促进下胚轴生长。我们证明 COP1 被 S-亚硝化，特别是在遮荫下。破坏这种氧化还原调节会增强蛋白酶体对 COP1 的降解，并降低 COP1 与靶蛋白相互作用和促进下胚轴生长的能力。这种调节的失活也会在下胚轴生长中产生横向不对称，表明不同细胞之间的协调不良，这导致随机的下胚轴弯曲和可预测的低竞争能力与邻居。这些发现强调了氧化还原信号在遮荫回避过程中控制扩散生长的重要性。
