Cell Reports e p 3

of somatic disorders determined by the mutation, its prevalence in the tissue, and the time point during development when sorting (FACS) as previously described (Evrony et al., 2012), us-ing NeuN immunoreactivity to identify neurons, and comprehen-sively compared MDA and GenomePlex. Single neuronal nucleithe mutation occurred (Poduri et al., 2013). Single-nucleotide variants (SNVs) and copy-number variants (CNVs) arising during or pooled 100-neuronal nuclei samples from three normal adult human brains (UMB1465, UMB4638, and UMB4643), oneomy 1q in 20 % of neurons, suggesting that CNVs in a minority of cells can cause widespread brain dysfunction. Single-cell analysis identified large (>1 Mb) clonal CNVs in lymphoblasts and in single neurons from normal human brain tissue, suggesting that some CNVs occur during neurogenesis. Many neurons contained one or more large candidate pri-vate CNVs, including one at chromosome 15q13.2-13.3, a site of duplication in neuropsychiatric conditions. Large private and clonal somatic CNVs occur in normal and diseased human brains