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• W2997384029 abstract "Summary Unrepaired DNA damage during embryonic development can be potentially inherited by a large population of cells. However, the quality control mechanisms that minimize the contribution of damaged cells to developing embryos remain poorly understood. Here, we uncovered an ATR- and CHK1-mediated transcriptional response to replication stress (RS) in ESCs that induces genes expressed in totipotent two-cell (2C) stage embryos and 2C-like cells. This response is mediated by Dux, a multicopy retrogene defining the cleavage-specific transcriptional program in placental mammals. In response to RS, DUX triggers the transcription of 2C-like markers such as murine endogenous retrovirus-like elements (MERVL) and Zscan4. This response can also be elicited by ETAA1-mediated ATR activation in the absence of RS. ATR-mediated activation of DUX requires GSRF1 dependent post-transcriptional regulation of Dux mRNA. Strikingly, activation of ATR expands ESCs fate potential by extending their contribution to both embryonic and extra­embryonic tissues. These findings define a novel ATR dependent pathway involved in maintaining genome stability in developing embryos by controlling ESCs fate in response to RS." @default.
• W2997384029 created "2020-01-10" @default.
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• W2997384029 date "2020-01-01" @default.
• W2997384029 modified "2023-10-18" @default.
• W2997384029 title "ATR expands embryonic stem cell fate potential in response to replication stress" @default.
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• W2997384029 doi "https://doi.org/10.1101/2020.01.01.888354" @default.
• W2997384029 hasPublicationYear "2020" @default.
• W2997384029 type Work @default.
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