Somatic mutation in single human neurons tracks developmental and transcriptional history
Author(s) -
Michael A. Lodato,
Mollie B. Woodworth,
Semin Lee,
Gilad D. Evrony,
Bhaven K. Mehta,
Amir Karger,
Soohyun Lee,
Thomas W. Chittenden,
Alissa M. D’Gama,
Xuyu Cai,
Lovelace J. Luquette,
Eunjung Lee,
Peter J. Park,
Christopher A. Walsh
Publication year - 2015
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.aab1785
Subject(s) - somatic cell , biology , germline , germline mutation , mutation , genetics , cerebral cortex , gene , genome , human brain , lineage (genetic) , neuroscience
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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