| dc.description.abstract | In addition to heat stress, an amino acid analog azetidine-2-carboxylic acid (AZC) is shown to induce production of unfolded or misfolded proteins in overall cells. Hence, the unfolded protein response (UPR), which is induced by the accumulation of misfolded proteins in the endoplasmic reticulum (ER), recruits specific genes and pathways to regulate protein repair in that compartment, and a parallel process, the cytosolic protein response (CPR), operates in the cytosol. The CPR is associated with the induction of a specific subset of HSP genes. In previous study, we found that Oshsp17.3 was expressed in Arabidopsis system under AZC treatment. In this study, we plan to use this system to detect which AtHSFs involved in CPR. RT-PCR analysis showed that the AtHSFA2, AtHSFA4a, AtHSFA7a, AtHSFB2a and AtHSFB2b were significantly induced by AZC. Thus we transfer the promoter of Oshsp17.3, which shows AZC responsiveness, fused with GUS reporter gene into these Arabidopsis hsf mutants and compare their GUS activity under AZC treatment. First, the RT-PCR analysis showed that the expression of other AtHSFs in the single or double athsf mutants were not significantly influenced by AZC treatment. Second, in the GUS activity analysis, we found that the GUS activity of Oshsp17.3pro::GUS was repressed in athsfA2, athsfA4a, athsfA7a, athsfB2a and athsfB2b mutants. Third, the RT-PCR analysis showed that AtHSFs were not activation under Tunicamycin treatment, which is an inducer of UPR. Hence, we suggest that these HSFs may involve in the regulation of the expression of Oshsp17.3 under AZC treatment. In these HSFs, AtHSFA2 may play a major role in the CPR of Arabidopsis in response to AZC treatment. | en_US |