NAC062 acts as an upstream regulator of NAC103 under endoplasmic reticulum stress

Abstract Environmental stresses may trigger the accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER), thus leading to ER stress in plants. Endoplasmic reticulum stress, harmful to plant growth, can be alleviated by upregulating unfolded protein response (UPR) initiated by transcription factors. NAC062 and NAC103, as reported in previous studies, both play significant roles in upregulating UPR genes to promote cell survival under ER stress in Arabidopsis . It is still unclear, however, which one of them acts as an upstream regulator in the ER stress pathway. Results of the current study demonstrated that NAC062 acts as an upstream regulator to directly regulate the expression of NAC103 to mediate ER stress in mouse‐ear cress [ Arabidopsis thaliana (L.) Heynh]. The expression of NAC103 is upregulated by the overexpression of NAC062D (the nuclear localization form of NAC062). Through subsequent dual‐luciferase reporter assay and yeast one‐hybrid (YIH) assay, NAC062D was found directly bound to the NAC103 promoter. The results of real‐time reverse transcription polymerase chain reaction (qRT‐PCR) showed that NAC062 and NAC103 are both upregulated in biotic stress (jasmonic acid [JA] treatment) and abiotic stress (such as salt stress, oxidation stress, and cold stress) pathways. Studying the relationship between NAC062 and NAC103 is beneficial to understand their function in biotic and abiotic stress pathways, so as to enhance plants tolerance under environmental stresses.