作者: Naoki Ogawa , Kazutoshi Mori
DOI: 10.1111/J.1365-2443.2004.00704.X
关键词:
摘要: Eukaryotic cells respond to the accumulation of unfolded proteins in endoplasmic reticulum (ER) by activating a transcriptional induction program termed protein response (UPR). The transcription factor Hac1p responsible for UPR Saccharomyces cerevisiae is tightly regulated post-transcriptional mechanism. HAC1 mRNA must be spliced ER stress produce Hac1p, which then activates via direct binding cis-acting element (UPRE) present promoter regions its target genes. Here, we show that itself responds induce downstream gene, similarly KAR2 promoter; gene represents major UPR. Consistent with this observation, contains an UPRE-like sequence, necessary and sufficient binds directly. Cells expressing from mutant lacking UPRE could not maintain high levels either unspliced or became sensitive when insulted hours. Based on these results, concluded autoregulation genes required sustained activation resistance stress.