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首页> 外文期刊>Genetics: A Periodical Record of Investigations Bearing on Heredity and Variation >The Oxidative Stress Response in Caenorhabditis elegans Requires the GATA Transcription Factor ELT-3 and SKN-1/Nrf2
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The Oxidative Stress Response in Caenorhabditis elegans Requires the GATA Transcription Factor ELT-3 and SKN-1/Nrf2

机译：Caenorhabditis elefars的氧化应激反应需要Gata转录因子ELT-3和SKN-1 / NRF2

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摘要

Cellular damage caused by reactive oxygen species is believed to be a major contributor to age-associated diseases. Previously, we characterized the Caenorhabditis elegans Brap2 ortholog (BRAP-2) and found that it is required to prevent larval arrest in response to elevated levels of oxidative stress. Here, we report that C. elegans brap-2 mutants display increased expression of SKN-1-dependent, phase II detoxification enzymes that is dependent on PMK-1 (a p38 MAPK C. elegans ortholog). An RNA-interference screen was conducted using a transcription factor library to identify genes required for increased expression of the SKN-1 target gst-4 in brap-2 mutants. We identified ELT-3, a member of the GATA transcription factor family, as a positive regulator of gst-4p::gfp expression. We found that ELT-3 interacts with SKN-1 to activate gst-4 transcription in vitro and that elt-3 is required for enhanced gst-4 expression in the brap-2(ok1492) mutant in vivo. Furthermore, nematodes overexpressing SKN-1 required ELT-3 for life-span extension. Taken together, these results suggest a model where BRAP-2 acts as negative regulator of SKN-1 through inhibition of p38 MAPK activity, and that the GATA transcription factor ELT-3 is required along with SKN-1 for the phase II detoxification response in C. elegans.
机译：由反应性氧物质引起的细胞损伤被认为是年龄相关疾病的主要因素。以前，我们以CaenorhabdisegrisBrap2 Ortholog（BRAP-2）为特征，发现需要防止幼虫抑制氧化胁迫水平的升高。在这里，我们报告说秀丽隐杆线虫BRAP-2突变体显示出依赖于PMK-1的SKN-1依赖性的II期解毒酶的增加（P38 MAPK C. Elegans Ortholog）。使用转录因子文库进行RNA干扰筛网，以鉴定BRAP-2突变体中SKN-1靶GST-4的表达增加所需的基因。我们鉴定了ELT-3，GATA转录因子家族的成员，作为GST-4P :: GFP表达的正调节因子。我们发现ELT-3与SKN-1相互作用以在体外激活GST-4转录，并且ELT-3需要在体内BAP-2（OK1492）突变体中增强的GST-4表达。此外，对于寿命延伸，对SKN-1的线虫提供过度抑制的SKN-1所需的ELT-3。总之，这些结果表明BRAP-2通过抑制P38 MAPK活性作为SKN-1的负调节剂的模型，并且GATA转录因子ELT-3是必需的，用于SKN-1用于II期解毒反应C.秀丽隐形。

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