Journal
SCIENCE
Volume 350, Issue 6256, Pages 94-98Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aab1785
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Funding
- National Center for Research Resources [1S10RR028832-01]
- National Institute on Aging [T32 AG000222]
- Leonard and Isabelle Goldenson Research Fellowship
- National Institute of General Medical Sciences (NIGMS) [T32 GM007753]
- Louis Lange III Scholarship in Translational Research
- NIGMS [T32 GM007753, T32 GM007226]
- Eleanor and Miles Shore Fellowship
- National Institute of Mental Health [P50 MH106933]
- National Institute of Neurological Disorders and Stroke [R01 NS032457, R01 NS079277, U01 MH106883]
- Manton Center for Orphan Disease Research
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Neurons live for decades in a postmitotic state, their genomes susceptible to DNA damage. Here we survey the landscape of somatic single-nucleotide variants (SNVs) in the human brain. We identified thousands of somatic SNVs by single-cell sequencing of 36 neurons from the cerebral cortex of three normal individuals. Unlike germline and cancer SNVs, which are often caused by errors in DNA replication, neuronal mutations appear to reflect damage during active transcription. Somatic mutations create nested lineage trees, allowing them to be dated relative to developmental landmarks and revealing a polyclonal architecture of the human cerebral cortex. Thus, somatic mutations in the brain represent a durable and ongoing record of neuronal life history, from development through postmitotic function.
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