Accumulation of cadmium (Cd) in rice is not only harmful to the growth of plants but also poses a threat to human health. Exposure to Cd triggers unfolded protein response (UPR) within cells, a process that is still not completely understood. The study demonstrated that the lack of OsbZIP39, an essential endoplasmic reticulum (ER)-resident regulator of the UPR, resulted in decreased Cd intake and reduced Cd levels in the roots, stems, and grains of rice. Upon exposure to Cd stress, GFP-OsbZIP39 translocated from ER to nucleus, initiating UPR. Further investigation revealed that Cd treatment caused changes in sphingolipid levels in the membrane, influencing the localization and activation of OsbZIP39. Yeast one-hybrid and dual-LUC assays were conducted to validate the interaction between activated OsbZIP39 and the promoter of the defensin-like gene , resulting in an increase in its expression. Different variations were identified in the coding region of , which may explain the varying levels of Cd accumulation observed in the and subspecies. Under Cd treatment, OsbZIP39 exhibited a more significant enhancement in the transcription of compared to OsbZIP39. Our data suggest that OsbZIP39 positively regulates Cd uptake in rice, offering an encouraging objective for the cultivation of low-Cd rice.

中文翻译：

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内质网应激反应调节剂OsbZIP39通过激活水稻中防御素样基因OsCAL2的表达来调节镉的积累


大米中镉（Cd）的积累不仅对植物生长有害，而且对人体健康构成威胁。暴露于镉会触发细胞内的未折叠蛋白反应（UPR），这一过程尚未完全了解。研究表明，OsbZIP39（UPR 的必需内质网 (ER) 驻留调节因子）的缺乏会导致水稻根、茎和籽粒中镉摄入量的减少以及镉水平的降低。暴露于 Cd 胁迫后，GFP-OsbZIP39 从 ER 转移到细胞核，启动 UPR。进一步的研究表明，镉处理引起膜中鞘脂水平的变化，影响 OsbZIP39 的定位和激活。进行酵母单杂交和双 LUC 测定，以验证激活的 OsbZIP39 和防御素样基因启动子之间的相互作用，从而导致其表达增加。在 的编码区中发现了不同的变异，这可以解释在 和 亚种中观察到的镉积累水平的不同。在Cd处理下，与OsbZIP39相比，OsbZIP39表现出更显着的转录增强。我们的数据表明，OsbZIP39 积极调节水稻中的镉吸收，为低镉水稻的种植提供了令人鼓舞的目标。