Dysregulation of let-7 by PEG modified graphene oxide in nematodes with deficit in epidermal barrier
Dysregulation of let-7 by PEG modified graphene oxide in nematodes with deficit in epidermal barrier
复制标题
PEG修饰的氧化石墨烯对表皮屏障缺陷的线虫中let-7的失调
DOI：
10.1016/j.ecoenv.2018.10.106
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发表时间：
2019
影响因子：
6.8
通讯作者：
Wang Dayong
中科院分区：
文献类型：
--
作者：
Zhao Li;Dong Shuangshuang;Zhao Yunli;Shao Huimin;Krasteva Natalia;Wu Qiuli;Wang Dayong
在秀丽隐杆线虫中，表皮RNA干扰（RNAi）敲低编码表皮胶原蛋白的bli-1，引起GO-PEG（PEG表面修饰的氧化石墨烯）的毒性诱导。在本研究中，我们进一步发现表皮RNAi敲除bli-1后，microRNAlet-7的表达增加，let-7突变可抑制bli-1（RNAi）线虫对GO-PEG毒性的敏感性，let-7通过抑制其直接靶点HBL-1和LIN-41的表达和功能来调节GO-PEG的毒性诱导。与bli-1表皮RNAi敲除线虫一样，hbl-1 orlin-41表皮RNAi敲除线虫也诱导表皮屏障功能异常。因此，BLI-1-let-7-HBL-1/LIN-41的信号级联被提出参与GO-PEG毒性诱导。我们的数据表明，在由bli-1（RNAi）引起的表皮屏障缺陷的线虫中，GO-PEG对let-7介导的发育时序控制分子机制的失调。
In nematode Caenorhabditis elegans, epidermal RNA interference (RNAi) knockdown ofbli-1encoding a cuticular collagen caused the toxicity induction of GO-PEG (PEG surface modified graphene oxide). In this study, we further found that epidermal RNAi knockdown ofbli-1increased expression of a microRNAlet-7, andlet-7mutation suppressed the susceptibility ofbli-1(RNAi)nematodes to GO-PEG toxicity.let-7regulated the toxicity induction of GO-PEG by suppressing expression and function of its direct targets (HBL-1 and LIN-41). Like the nematodes with epidermal RNAi knockdown ofbli-1, epidermal RNAi knockdown ofhbl-1orlin-41also induced functional abnormality in epidermal barrier. Therefore, a signaling cascade of BLI-1-let-7-HBL-1/LIN-41 was raised to be involved in GO-PEG toxicity induction. Our data imply the dysregulation oflet-7-mediated molecular machinery for developmental timing control by GO-PEG in nematodes with deficit in epidermal barrier caused bybli-1(RNAi).