Radioadaptive Response for Reproductive Cell Death Demonstrated in In Vivo Tissue Model of Caenorhabditis elegans
Radioadaptive Response for Reproductive Cell Death Demonstrated in In Vivo Tissue Model of Caenorhabditis elegans
复制标题
DOI：
10.1667/rr14368.1
复制
发表时间：
2016-03
影响因子：
3.4
通讯作者：
Huangqi Tang;Liangwen Chen;Jialu Liu;Jue Shi;Qingqing Li;Ting Wang;Lijun Wu;Furu Zhan;P. Bian
中科院分区：
文献类型：
--
作者：
Huangqi Tang;Liangwen Chen;Jialu Liu;Jue Shi;Qingqing Li;Ting Wang;Lijun Wu;Furu Zhan;P. Bian
生殖细胞死亡（RCD）发生在一次或多次细胞分裂后，这些细胞分裂是由辐射暴露或其他致癌物或诱变剂处理引起的。RCD的放射适应性反应通常通过体外或体内克隆形成试验来研究。到目前为止，这还没有在秀丽隐杆线虫的外阴组织中得到证实。elegans），其是辐射诱导的RCD的良好建立的体内模型。本研究旨在确定在C.线虫早期幼虫用较低的适应剂量进行伽马辐照，然后用较高的攻击剂量进行辐照。以外阴突出率作为评价外阴细胞RCD的指标。本研究结果表明，在生殖道发育14-16 h的时间点，5 + 75戈伊和5 + 100戈伊的剂量组合可诱导生殖道组织模型对RCD产生良好的辐射适应性反应。此外，时间过程分析表明，外阴细胞的辐射抗性在适应剂量后1.75小时内发展，并持续很短的时间（2 - 4小时）。DNA损伤检查点和非同源末端连接参与了辐射适应性反应，表现出在这两个途径中缺乏的蠕虫与其对照相似的外阴突出诱导。有趣的是，DNA损伤检查点在体细胞外阴细胞中不活跃，因此，DNA损伤检查点可能以细胞非自主的方式介导辐射适应性反应。在这里，我们展示了在C的外阴组织模型中RCD发生放射适应性反应的证据。优雅的这一发现提供了一个潜在的机会，进一步了解辐射适应性反应的RCD的潜在机制，鉴于C。优美的
Reproductive cell death (RCD) occurs after one or more cell divisions resulting from an insult such as radiation exposure or other treatments with carcinogens or mutagens. The radioadaptive response for RCD is usually investigated by in vitro or in vivo clonogenic assay. To date, this has not been demonstrated in the vulval tissue in Caenorhabditis elegans (C. elegans), which is a well established in vivo model for radiation-induced RCD. In this study to determine whether radioadaptive response occurs in the vulval tissue model of C. elegans, early larval worms were gamma irradiated with lower adaptive doses, followed by higher challenge doses. The ratio of protruding vulva was used to assess the RCD of vulval cells. The results of this study showed that the radioadaptive response for RCD in this vulval tissue model could be well induced by dose combinations of 5 + 75 Gy and 5 + 100 Gy at the time point of 14–16 h in worm development. In addition, the time course analysis indicated that radioresistance in vulval cells developed within 1.75 h after an adaptive dose and persisted for only a short period of time (2–4 h). DNA damage checkpoint and non-homologous end joining were involved in the radioadaptive response, exhibiting induction of protruding vulva in worms deficient in these two pathways similar to their controls. Interestingly, the DNA damage checkpoint was not active in the somatic vulval cells, and it was therefore suggested that the DNA damage checkpoint might mediate the radioadaptive response in a cell nonautonomous manner. Here, we show evidence of the occurrence of a radioadaptive response for RCD in the vulval tissue model of C. elegans. This finding provides a potential opportunity to gain further insight into the underlying mechanisms of the radioadaptive response for RCD, in view of the abundant genetic resources of C. elegans.