Detienne Giel, Van de Walle Pieter, De Haes Wouter, Schoofs Liliane, Temmerman Liesbet
Department of Biology , KU Leuven , Leuven, Belgium.
Worm. 2016 Aug 31;5(4):e1230585. doi: 10.1080/21624054.2016.1230585. eCollection 2016.
In research, transcriptional activation of glutathione S-transferase 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 promoter to SKN-1, this is also often ignored. We here show that 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 transcription in response to augmented EGF signaling. Our findings caution researchers within the community to always rely on sufficient experimental controls when assaying SKN-1 transcriptional activity with a reporter, such as SKN-1 loss-of-function mutants and/or additional target genes next to .
在研究中,谷胱甘肽S-转移酶4()的转录激活常被用作SKN-1活性的读数。虽然许多人注意到由启动子驱动的绿色荧光蛋白报告信号对SKN-1的假定非排他性,但这一点也常常被忽视。我们在此表明,EOR-1也可以转录激活,EOR-1是一种介导表皮生长因子(EGF)途径效应的转录因子。除了增强对外源氧化应激的耐受性外,EOR-1独立于SKN-1增加转录以响应增强的EGF信号。我们的发现提醒该领域的研究人员,在用报告基因(如SKN-1功能丧失突变体和/或旁边的其他靶基因)测定SKN-1转录活性时,始终要依靠充分的实验对照。