Abstract
Poly(PR), a toxic dipeptide-repeat protein, translated from the pathogenic G4C2 repeat expansion in C9orf72, contributes to c9 amyotrophic lateral sclerosis/frontotemporal dementia (c9ALS/FTD). However, precisely how poly(PR) elicits neurodegeneration has remained unclear. Maor-Nof et al. now establish that poly(PR) remodels the neuronal epigenome to promote proapoptotic p53 activity involving PUMA, which drives neurodegeneration in several models.
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