| Literature DB >> 35901164 |
Taejeong Bae1, Liana Fasching2, Yifan Wang1, Joo Heon Shin3,4, Milovan Suvakov1, Yeongjun Jang1, Scott Norton2, Caroline Dias5,6, Jessica Mariani2, Alexandre Jourdon2, Feinan Wu2, Arijit Panda1, Reenal Pattni7, Yasmine Chahine5,6, Rebecca Yeh5,6, Rosalinda C Roberts8, Anita Huttner9, Joel E Kleinman3,10, Thomas M Hyde3,4,10, Richard E Straub3, Christopher A Walsh5,6, Alexander E Urban7, James F Leckman2, Daniel R Weinberger3,4,10,11,12, Flora M Vaccarino2,13, Alexej Abyzov1.
Abstract
We analyzed 131 human brains (44 neurotypical, 19 with Tourette syndrome, 9 with schizophrenia, and 59 with autism) for somatic mutations after whole genome sequencing to a depth of more than 200×. Typically, brains had 20 to 60 detectable single-nucleotide mutations, but ~6% of brains harbored hundreds of somatic mutations. Hypermutability was associated with age and damaging mutations in genes implicated in cancers and, in some brains, reflected in vivo clonal expansions. Somatic duplications, likely arising during development, were found in ~5% of normal and diseased brains, reflecting background mutagenesis. Brains with autism were associated with mutations creating putative transcription factor binding motifs in enhancer-like regions in the developing brain. The top-ranked affected motifs corresponded to MEIS (myeloid ectopic viral integration site) transcription factors, suggesting a potential link between their involvement in gene regulation and autism.Entities:
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Year: 2022 PMID: 35901164 PMCID: PMC9420557 DOI: 10.1126/science.abm6222
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 63.714