P53 is a central regulator driving neurodegeneration caused by C9orf72 poly(PR)
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ABSTRACT: To analyze the epigenomic landscape of neurodegeneration caused by ALS-associated protein aggregation, we developed a modified version of ATAC-seq that works on primary neurons. We discovered that C9orf72-ALS/FTD associated poly(PR) activated a remarkably specific signature of chromatin accessibility, involving transcriptional targets of the tumor suppressor gene p53. Our findings reveal an unexpected role of p53 as a mediator of neurodegeneration elicited by poly(PR) and provide an example of how ATAC-seq can now be applied to neurons to define mechanisms of neurodegeneration.
ORGANISM(S): Mus musculus Homo sapiens
PROVIDER: GSE162048 | GEO | 2020/12/09
REPOSITORIES: GEO
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