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An integrated genome-wide resource of DSBs, DNA replication, replication timing, transcription, and R-loops in two widely used cancer cell lines, under steady-state conditions and following prolonged low-dose DNA polymerase inhibition is established.
A model in which WWOX mutations impair neurogenesis via RG through cell-type specific dysregulation of the MYC and Wnt signaling pathways is proposed, highlighting potential therapeutic strategies for WWOX-related disorders and open avenues for interventions targeting these key molecular pathways.
These findings establish DLG4 haploinsufficiency as a shared consequence of pathogenic DLG4 variants, while revealing additional variant-associated effects on neuronal structure and activity, rescued by AAV9-mediated neuronal restoration.
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