Aug 28, 2014

Incorporation of a nucleoside analog maps genome repair sites in post-mitotic human neurons

Jenny TungFred H. Gage


Neurons are the longest-living cells in our bodies, becoming post-mitotic in early development upon terminal differentiation. Their lack of DNA replication makes them reliant on DNA repair mechanisms to maintain genome fidelity. These repair mechanisms decline with age, potentially giving rise to genomic dysfunction that may influence cognitive decline and neurodegenerative diseases. Despite this challenge, our knowledge of how genome instability emerges and what mechanisms neurons and other long-lived cells may have evolved to protect their genome integrity over the human life span is limited. Using a targeted sequencing approach, we demonstrate that neurons consolidate much of their DNA repair efforts into well-defined hotspots that protect genes that are essential for their identity and function. Our findings provide a basis to understand genome integrity as it relates to aging and disease in the nervous system.

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Mentioned in this Paper

Quantitative Trait Loci
Nonhuman primate
Sequence Determinations, RNA
Dysequilibrium Syndrome
Gene Expression

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