Comprehensive multi-omic profiling of somatic mutations in malformations of cortical development.
Changuk ChungXiaoxu YangTaejeong BaeKeng Ioi VongSwapnil MittalCatharina DonkelsH Westley PhillipsZhen LiAshley P L MarshMartin W BreussLaurel L BallCamila Araújo Bernardino GarciaRenee D GeorgeJing GuMingchu XuChelsea BarrowsKiely N JamesValentina StanleyAnna S NidhirySami KhouryGabrielle HoweEmily RileyXin XuBrett CopelandYifan WangSe-Hoon KimHoon-Chul KangAndreas Schulze-BonhageCarola A HaasHorst UrbachMarco PrinzDavid D LimbrickChristina A GurnettMatthew D SmythShifteh SattarMark NespecaDavid D GondaKatsumi ImaiYukitoshi TakahashiHsin-Hung ChenJin-Wu TsaiValerio ContiRenzo GuerriniOrrin DevinskyWilson Araújo da Silva JuniorHelio R MachadoGary W MathernAlexej AbyzovSara BaldassariStéphanie Baulacnull nullnull nullJoseph G GleesonPublished in: Nature genetics (2023)
Malformations of cortical development (MCD) are neurological conditions involving focal disruptions of cortical architecture and cellular organization that arise during embryogenesis, largely from somatic mosaic mutations, and cause intractable epilepsy. Identifying the genetic causes of MCD has been a challenge, as mutations remain at low allelic fractions in brain tissue resected to treat condition-related epilepsy. Here we report a genetic landscape from 283 brain resections, identifying 69 mutated genes through intensive profiling of somatic mutations, combining whole-exome and targeted-amplicon sequencing with functional validation including in utero electroporation of mice and single-nucleus RNA sequencing. Genotype-phenotype correlation analysis elucidated specific MCD gene sets associated with distinct pathophysiological and clinical phenotypes. The unique single-cell level spatiotemporal expression patterns of mutated genes in control and patient brains indicate critical roles in excitatory neurogenic pools during brain development and in promoting neuronal hyperexcitability after birth.
Keyphrases
- single cell
- copy number
- genome wide
- rna seq
- resting state
- cerebral ischemia
- genome wide identification
- white matter
- high throughput
- dna methylation
- functional connectivity
- poor prognosis
- spinal cord injury
- transcription factor
- lymph node
- brain injury
- adipose tissue
- gene expression
- cancer therapy
- wild type
- metabolic syndrome
- long non coding rna
- skeletal muscle
- data analysis