In this paper, we uncover a damaged chromatin marking mechanism that drives the non-random segregation of UV damage through mitosis with potential consequences on daughter cell fate. Thus, we reveal that chromatin alterations impinge on genome stability not only by regulating DNA repair but also by controlling DNA damage segregation, which broadens the scope of genome maintenance mechanisms.
For more details, see Ferrand*, Dabin* et al., Nat Commun 2025.
Working model for how UV-damaged chromatin marking through alteration of mitotic histone phosphorylation controls the segregation of DNA damage in the cell progeny with consequences on daughter cell fate.
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