Essential role of poly(ADP-ribosyl)ation in maintenance of spermatogonial stem cells

精原干细胞（SSCs）在体外存在胶质细胞系来源的神经营养因子（SSCs的自我更新因子）的情况下可以增殖。这些培养的ssc被称为种系干细胞（GS）。在之前的研究中，我们检测了PARP抑制剂（poly(ADP-ribosyl)）的抑制作用对GS细胞的影响。抑制聚adp -核糖基化抑制GS细胞增殖，诱导细胞死亡。为了确定参与抑制细胞增殖途径的致病基因，我们进行了基因表达和蛋白磷酸化分析。加入PARP抑制剂后，p53信号通路部分基因表达上调。然后，我们通过检测其磷酸化位点来研究p53的激活。加入PARP抑制剂后，磷酸化程度增加。这些结果表明，聚（adp -核糖基）化调节了GS细胞中p53的活性，从而调节了p53信号通路。

Spermatogonial stem cells (SSCs) can proliferate in vitro in the presence of glial cell line-derived neurotrophic factor, a self-renewal factor for SSCs. These cultured SSCs are called germline stem (GS) cells. In previous study, we examined the effect of PARP inhibitor, inhibition of poly(ADP-ribosyl)ation, on GS cells. Inhibition of poly(ADP-ribosyl)ation suppressed cell proliferation of GS cells, and induced cell death. In order to identify the causative genes that is involved in the pathway leading to the suppression of cell proliferation, the gene expression and protein phosphorylation analyses were carried out. Some genes in p53 signaling pathway were up-regulated after addition of PARP inhibitors. We then investigated activation of p53 by detection of its phosphorylation site. The phosphorylation was increased after addition of PARP inhibitors. These results suggest that poly(ADP-ribosyl)ation regulates activity of p53 and thus p53 signaling pathway in GS cells.