H₂O₂ affects the expression of genes that are involved in plant responses to diverse environmental stresses; however, the underlying mechanisms remain elusive. Here, we demonstrate that H₂O₂ enhances plant freezing tolerance through its effect on a protein product of low expression of osmotically responsive genes2 (LOS2). LOS2 is translated into a major product, cytosolic enolase2 (ENO2), and sometimes an alternative product, the transcription repressor c-Myc-binding protein (MBP-1). ENO2, but not MBP-1, promotes cold tolerance by binding the promoter of C-repeat/DRE binding factor1 (CBF1), a central transcription factor in plant cold signaling, thus activating its expression. Overexpression of CBF1 restores freezing sensitivity of a LOS2 loss-of-function mutant. Furthermore, cold-induced H₂O₂ increases nuclear import and transcriptional binding activity of ENO2 by sulfenylating cysteine 408 and thereby promotes its oligomerization. Collectively, our results illustrate how H₂O₂ activates plant cold responses by sulfenylating ENO2 and promoting its oligomerization, leading to enhanced nuclear translocation and transcriptional activation of CBF1.

H ₂ O ₂影响与植物对不同环境胁迫的反应有关的基因的表达；然而，潜在的机制仍然难以捉摸。在这里，我们证明 H ₂ O ₂通过其对渗透响应基因 2 ( LOS2 )低 表达的蛋白质产物的影响来增强植物的抗冻性。LOS2被翻译成主要产物，胞质烯醇化酶2 (ENO2)，有时还被翻译成替代产物，转录抑制因子 c-Myc 结合蛋白 (MBP-1)。ENO2，但不是 MBP-1，通过结合C-重复/DRE 结合因子1 的启动子（CBF1)，植物冷信号中的中心转录因子，从而激活其表达。CBF1的过表达恢复了LOS2功能丧失突变体的冷冻敏感性。此外，冷诱导的 H ₂ O ₂通过对半胱氨酸 408 进行亚磺酰化来增加 ENO2 的核输入和转录结合活性，从而促进其寡聚化。总的来说，我们的结果说明了 H ₂ O ₂如何通过使 ENO2 亚硫基化并促进其寡聚化来激活植物的低温反应，从而增强CBF1的核转位和转录激活。