Oxidative stress causes damage to cells by creating reactive oxygen species (ROS) and the overproduction of ROS have been linked to the onset of premature aging. We previously found that a brap-2 (BRCA1 associated protein 2) mutant significantly increases the expression of phase II detoxification enzymes in C. elegans. An RNAi suppression screen to identify transcription factors involved in the production of gst-4 mRNA in brap-2 worms identified SEM-4 as a potential candidate. Here, we show that knockdown of sem-4 suppresses the activation of gst-4 caused by the mutation in brap-2. We also demonstrate that sem-4 is required for survival upon exposure to oxidative stress and that SEM-4 is required for expression of the transcription factor SKN-1C. These findings identify a novel role for SEM-4 in ROS detoxification by regulating expression of SKN-1C and the phase II detoxification genes.

氧化应激会通过产生活性氧（ROS）导致细胞受损，并且ROS的过度产生与过早衰老的发生有关。我们先前发现brap-2（BRCA1相关蛋白2）突变体显着增加了秀丽隐杆线虫II期解毒酶的表达。RNAi抑制筛选可识别参与生产RNAi的转录因子GST-4 mRNA在 brap-2 确定的蠕虫 扫描电镜4作为潜在的候选人。在这里，我们表明sem-4 抑制激活 GST-4 由突变引起 brap-2。我们还证明了sem-4被曝光时需要生存氧化应激和扫描电镜4表达转录因子SKN-1C是必需的。这些发现确定了新的作用SEM-4通过调节SKN-1C和II期排毒基因的表达来进行ROS排毒。