Various stresses can affect the quality and yield of crops, including vegetables. In this study, CRISPR/Cas9 technology was employed to examine the role of the ELONGATED HYPOCOTYL 5 (HY5) gene in influencing the growth of Chinese cabbage (Brassica rapa). Single guide RNAs (sgRNAs) were designed to target the HY5 gene, and deep-sequencing analysis confirmed the induction of mutations in the bZIP domain of the gene. To investigate the response of Chinese cabbage to endoplasmic reticulum (ER) stress, plants were treated with tunicamycin (TM). Both wild-type and hy5 mutant plants showed increased growth inhibition with increasing TM concentration. However, the hy5 mutant plants displayed less severe growth inhibition compared to the wild type. Using nitroblue tetrazolium (NBT) and 3,3′-diaminobenzidine (DAB) staining methods, we determined the amount of reactive oxygen species (ROS) produced under ER stress conditions, and found that the hy5 mutant plants generated lower levels of ROS compared to the wild type. Under ER stress conditions, the hy5 mutant plants exhibited lower expression levels of UPR- and cell death-related genes than the wild type. These results indicate that CRISPR/Cas9-mediated editing of the HY5 gene can mitigate growth inhibition in Chinese cabbage under stresses, improving the quality and yield of crops.

The endoplasmic reticulum (ER) must coordinate protein entry, maturation and removal to sustain plant growth and stress adaptation. Although unfolded protein response (UPR) signaling and quality control pathways are well characterized, their activation alone does not reveal which process limits ER function. Here, we propose a Load, Capacity and Clearance (LCC) framework that organizes these mechanisms by their effects on protein flux. The Load module regulates protein influx, Capacity supports productive folding, maturation, assembly and export, and Clearance removes misfolded proteins and selected portions of the ER. We examine transcriptional remodeling, translational regulation, regulated RNA decay, ER-associated degradation and selective autophagy, distinguishing mechanisms demonstrated during plant ER stress from those established in other stress responses. How these processes are coordinated, and how much each contributes to ER recovery, remain to be quantified. We outline testable predictions and experimental approaches to determine which processes limit recovery, how the timing of influx restoration affects recovery, and whether combined measurements of influx, processing and clearance explain or predict stress outcomes better than UPR markers alone. This framework may guide strategies to improve plant stress resilience and recombinant protein production.