Through dynamic activities of conserved master transcription factors (mTFs), the unfolded protein response (UPR) relieves proteostasis imbalance of the endoplasmic reticulum (ER), a condition known as ER stress^1,2. Because dysregulated UPR is lethal, the competence for fate changes of the UPR mTFs must be tightly controlled^3,4. However, the molecular mechanisms underlying regulatory dynamics of mTFs remain largely elusive. Here, we identified the abscisic acid-related regulator G-class bZIP TF2 (GBF2) and the cis-regulatory element G-box as regulatory components of the plant UPR led by the mTFs, bZIP28 and bZIP60. We demonstrate that, by competing with the mTFs at G-box, GBF2 represses UPR gene expression. Conversely, a gbf2 null mutation enhances UPR gene expression and suppresses the lethality of a bzip28 bzip60 mutant in unresolved ER stress. By demonstrating that GBF2 functions as a transcriptional repressor of the UPR, we address the long-standing challenge of identifying shared signalling components for a better understanding of the dynamic nature and complexity of stress biology. Furthermore, our results identify a new layer of UPR gene regulation hinged upon an antagonistic mTFs-GFB2 competition for proteostasis and cell fate determination.

通过保守的主转录因子 (mTF) 的动态活动，未折叠蛋白反应 (UPR) 减轻了内质网 (ER) 的蛋白质稳态失衡，这种情况称为 ER 应激^1,2。由于失调的 UPR 是致命的，因此必须严格控制 UPR mTF 命运变化的能力^3,4。然而，mTF 监管动态的分子机制在很大程度上仍然难以捉摸。在这里，我们将脱落酸相关调节剂 G 类 bZIP TF2 (GBF2) 和顺式调节元件 G-box 确定为由 mTF、bZIP28 和 bZIP60 领导的植物 UPR 的调节成分。我们证明，通过与 G-box 的 mTF 竞争，GBF2 抑制 UPR 基因表达。相反，一个gbf2无效突变增强了 UPR 基因表达并抑制了bzip28  bzip60突变体在未解决的 ER 应激中的杀伤力。通过证明 GBF2 作为 UPR 的转录抑制因子发挥作用，我们解决了识别共享信号成分的长期挑战，以便更好地理解应激生物学的动态性质和复杂性。此外，我们的结果确定了一个新的 UPR 基因调控层，该调控取决于对蛋白质稳态和细胞命运决定的拮抗性 mTFs-GFB2 竞争。