ArticleNucleic acids research2025
Ints7 deficiency activates DNA damage response to elicit resurgence of endogenous retrovirus MERVL and anastasis of embryonic stem cells.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The murine endogenous retrovirus MERVL is dynamically activated in a small population of in vitro cultured mouse embryonic stem cells (mESCs) exhibiting totipotent-like features. Yet, the relationship between MERVL activation and cell fate decisions of mESCs is incompletely understood. Through a genome-wide knockout screen, we discovered that MERVL activity is intrinsically linked to DNA damage response pathways. Loss of Ints7, a backbone subunit of the Integrator complex, increased DNA damage and triggered MERVL expression. Mechanistically, Ints7 depletion induced phosphorylation of Kap1, increased chromatin accessibility at MERVL loci, and activated the p53-Dux axis to drive MERVL transcription. Intriguingly, DNA damage-induced MERVL resurgence followed the cleavage of caspase-3, often accompanying a process known as anastasis-cell survival after transient apoptotic signaling. Collectively, our study uncovered that MERVL activation in mESCs is integrated into the cellular circuit for decision-making in response to DNA damage, suggesting that sublethal caspase activation can influence the developmental potential of stem cells.
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