First Affiliated Hospital, Zhejiang University School of Medicine, and Liangzhu Laboratory of Zhejiang University, Hangzhou, Zhejiang, China.
Institute of Hematology, Zhejiang University, Hangzhou, Zhejiang, China.
Cell Mol Life Sci. 2024 Oct 26;81(1):440. doi: 10.1007/s00018-024-05465-z.
The pluripotent mouse embryonic stem cell (mESCs) can transit into the totipotent-like state, and the transcription factor DUX is one of the master regulators of this transition. Intriguingly, this transition in mESCs is accompanied by massive cell death, which significantly impedes the establishment and maintenance of totipotent cells in vitro, yet the underlying mechanisms of this cell death remain largely elusive. In this study, we found that the totipotency transition in mESCs triggered cell death through the upregulation of DUX. Specifically, R-loops are accumulated upon DUX induction, which subsequently lead to DNA replication stress (RS) in mESCs. This RS further activates p53 and PMAIP1, ultimately leading to Caspase-9/7-dependent intrinsic apoptosis. Notably, inhibiting this intrinsic apoptosis not only mitigates cell death but also enhances the efficiency of the totipotency transition in mESCs. Our findings thus elucidate one of the mechanisms underlying cell apoptosis during the totipotency transition in mESCs and provide a strategy for optimizing the establishment and maintenance of totipotent cells in vitro.
多能性小鼠胚胎干细胞(mESCs)可以过渡到全能性样状态,转录因子 DUX 是这种转变的主要调控因子之一。有趣的是,mESCs 中的这种转变伴随着大量的细胞死亡,这极大地阻碍了体外全能性细胞的建立和维持,但这种细胞死亡的潜在机制在很大程度上仍难以捉摸。在这项研究中,我们发现 mESCs 中的全能性转变通过 DUX 的上调引发细胞死亡。具体来说,在 DUX 诱导后会积累 R-环,随后导致 mESCs 中的 DNA 复制应激(RS)。这种 RS 进一步激活 p53 和 PMAIP1,最终导致 Caspase-9/7 依赖性内在凋亡。值得注意的是,抑制这种内在凋亡不仅减轻了细胞死亡,而且还提高了 mESCs 全能性转变的效率。因此,我们的研究结果阐明了 mESCs 全能性转变过程中细胞凋亡的机制之一,并为优化体外全能性细胞的建立和维持提供了策略。