背景回顾：H2O₂ affects the expression of genes that are involved in plant responses to diverse environmental stresses; however, the underlying mechanisms remain elusive. 

主要发现：Here, we demonstrate that H2O₂ enhances plant freezing tolerance through its effect on a protein product of low expression of osmotically responsive genes2 (LOS2). 

结果1-LOS2编码ENO2和MBP-1：LOS2 is translated into a major product, cytosolic enolase2 (ENO2), and sometimes an alternative product, the transcription repressor c-Myc-binding protein (MBP-1). 

结果2-ENO2通过转录激活CBF1，增强抗冻性：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 CBF1restores freezing sensitivity of a LOS2 loss-of-function mutant. 

结果3-过氧化氢增强ENO2-CBF1模块：Furthermore, cold-induced H2O₂ increases nuclear import and transcriptional binding activity of ENO2 by sulfenylating cysteine 408 and thereby promotes its oligomerization. 

结论：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.

 摘 要 

过氧化氢影响参与植物响应多种环境胁迫相关基因的表达，但是潜在的分子机制并不清楚。本文中，作者发现过氧化氢能够通过其对于LOS2基因蛋白产物的影响，增强植物的抗冻性。LOS2基因主要编码一种胞质烯醇化酶ENO2，并且有时会发生可变剪切，编码一个转录抑制因子MBP-1。其中，ENO2能够通过结合到植物低温信号转导核心转录因子CBF1的启动子上，从而激活CBF1基因的表达，最终提升植物的低温抗性。过表达CBF1基因能够恢复LOS2功能缺失导致的低温敏感。此外，低温诱导的过氧化氢能够通过亚磺酸化ENO2蛋白408号位上的半胱氨酸，增强ENO2蛋白的入核能力及其转录结合活性，从而促进该蛋白的寡聚化。综上，本文的研究揭示了过氧化氢如何通过亚磺酸化ENO2蛋白以促进其寡聚化，从而增强ENO2蛋白的核转位及对CBF1基因的转录激活，最终激活植物的低温响应。

 袁红梅