SKN-1-independent transcriptional activation of glutathione S-transferase 4 (GST-4) by EGF signaling.
SKN-1-independent transcriptional activation of glutathione S-transferase 4 (GST-4) by EGF signaling.
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DOI：
10.1080/21624054.2016.1230585
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发表时间：
2016-01-01
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影响因子：
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通讯作者：
Temmerman, Liesbet
中科院分区：
文献类型：
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作者：
Detienne, Giel;Van de Walle, Pieter;Temmerman, Liesbet
在秀丽隐杆线虫研究中，谷胱甘肽 S-转移酶 4 (gst-4) 的转录激活通常用作 SKN-1 活性的读数。虽然许多人注意到 gst-4 启动子驱动的 GFP 报告信号对 SKN-1 的假设非排他性，但这也经常被忽视。我们在这里表明 gst-4 也可以被 EOR-1 转录激活，EOR-1 是一种介导表皮生长因子 (EGF) 途径作用的转录因子。除了增强外源氧化应激耐受性之外，EOR-1 独立于 SKN-1 还可以响应增强的 EGF 信号传导而增加 gst-4 转录。我们的研究结果提醒线虫群体内的研究人员，在使用 gst-4p::gfp 报告基因（例如 SKN-1 功能丧失突变体和/或 gst-4 旁边的其他靶基因）分析 SKN-1 转录活性时，始终依赖于足够的实验对照。
In C. elegans research, transcriptional activation of glutathione S-transferase 4 (gst-4) is often used as a read-out for SKN-1 activity. While many heed an assumed non-exclusivity of the GFP reporter signal driven by the gst-4 promoter to SKN-1, this is also often ignored. We here show that gst-4 can also be transcriptionally activated by EOR-1, a transcription factor mediating effects of the epidermal growth factor (EGF) pathway. Along with enhancing exogenous oxidative stress tolerance, EOR-1 inde-pendently of SKN-1 increases gst-4 transcription in response to augmented EGF signaling. Our findings caution researchers within the C. elegans community to always rely on sufficient experimental controls when assaying SKN-1 transcriptional activity with a gst-4p::gfp reporter, such as SKN-1 loss-of-function mutants and/or additional target genes next to gst-4.