10月19日《美国国家科学院院刊》杂志上发表南开大学陈凌懿教授研究团队揭示Erk信号对于小鼠ESC的自我更新调控机制的研究文章，陈海霞(Haixia Chen)为作者，论文通讯作者是南开大学生命科学学院陈凌懿教授和刘林教授。

南开大学生命科学学院陈凌懿教授和刘林教授的团队通过实验证明Erk信号在小鼠ESC的自我更新中起到了不可或缺的作用。研究指出，敲除了Erk的小鼠ESC无法维持。Erk缺乏导致多能性基因表达失调，细胞增殖速度减慢，细胞周期停滞于G1期，细胞凋亡增多，端粒快速缩短和基因组稳定性受损。

实验说明Erk信号对于小鼠ESC的自我更新非常关键，进一步研究表明，Mek其实具有不依赖Erk的功能。正因如此，Mek抑制和Erk敲除对ESC自我更新的影响并不相同。

原文链接：

Erk signaling is indispensable for genomic stability ａnd self-renewal of mouse embryonic stemCells

原文摘要：

Inhibition of Mek/Erk signaling by pharmacological Mek inhibitors promotes self-renewal ａnd pluripotency of mouse embryonic stem cells (ESCs). Intriguingly, Erk signaling is essential for human ESC self-renewal. Here we demonstrate that Erk signaling is critical for mouse ESC self-renewal ａnd genomic stability. Erk-depleted ESCs cannot be maintained. Lack of Erk leads to rapid telomere shortening ａnd genomic instability, in association with misregulated expression of pluripotency genes, reduced cell proliferation, G1 cell-cycle arrest, ａnd increased apoptosis. Erk signaling is also required for the activation of differentiation genes but not for the repression of pluripotency genes during ESC differentiation. Furthermore, we find an Erk-independent function of Mek, which may explain the diverse effects of Mek inhibition ａnd Erk knockout on ESC self-renewal. Together, in contrast to the prevailing view, Erk signaling is required for telomere maintenance, genomic stability, ａnd self-renewal of mouse ESCs.

doi: 10.1073/PNAS.1516319112