Journal
NEURON
Volume 89, Issue 6, Pages 1223-1236Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2016.02.004
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Funding
- National Institute on Deafness and Other Communication Disorders [DC012592]
- National Institute of Mental Health [MH102698]
- California Institute for Regenerative Medicine [RB3-02186]
- Baxter Family Foundation
- Norris Foundation
- Del Webb Foundation
- Las Patronas
- Dorris Neuroscience Center
- NIH [DP2OD006493-01]
- California Institute of Regenerative Medicine
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Somatic mutation in neurons is linked to neurologic disease and implicated in cell-type diversification. However, the origin, extent, and patterns of genomic mutation in neurons remain unknown. We established a nuclear transfer method to clonally amplify the genomes of neurons from adult mice for whole-genome sequencing. Comprehensive mutation detection and independent validation revealed that individual neurons harbor similar to 100 unique mutations from all classes but lack recurrent rearrangements. Most neurons contain at least one gene-disrupting mutation and rare (0-2) mobile element insertions. The frequency and gene bias of neuronal mutations differ from other lineages, potentially due to novel mechanisms governing postmitotic mutation. Fertile mice were cloned from several neurons, establishing the compatibility of mutated adult neuronal genomes with reprogramming to pluripotency and development.
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