학술논문

De Novo Coding Variants Are Strongly Associated with Tourette Disorder.
Document Type
article
Source
Neuron. 94(3)
Subject
Tourette International Collaborative Genetics
Tourette Syndrome Association International Consortium for Genetics
Humans
Tourette Syndrome
Genetic Predisposition to Disease
Intracellular Signaling Peptides and Proteins
Proteins
Cell Cycle Proteins
Fibronectins
Cadherins
Receptors
Cell Surface
Phosphoproteins
Odds Ratio
Cohort Studies
Sequence Analysis
DNA
Parents
Mutation
Adult
Child
Female
Male
Genetic Variation
TIC Genetics
TSAICG
Tourette disorder
Tourette syndrome
de novo variants
gene discovery
whole-exome sequencing
Biotechnology
Brain Disorders
Human Genome
Neurosciences
Clinical Research
Genetics
2.1 Biological and endogenous factors
Aetiology
Psychology
Cognitive Sciences
Neurology & Neurosurgery
Language
Abstract
Whole-exome sequencing (WES) and de novo variant detection have proven a powerful approach to gene discovery in complex neurodevelopmental disorders. We have completed WES of 325 Tourette disorder trios from the Tourette International Collaborative Genetics cohort and a replication sample of 186 trios from the Tourette Syndrome Association International Consortium on Genetics (511 total). We observe strong and consistent evidence for the contribution of de novo likely gene-disrupting (LGD) variants (rate ratio [RR] 2.32, p = 0.002). Additionally, de novo damaging variants (LGD and probably damaging missense) are overrepresented in probands (RR 1.37, p = 0.003). We identify four likely risk genes with multiple de novo damaging variants in unrelated probands: WWC1 (WW and C2 domain containing 1), CELSR3 (Cadherin EGF LAG seven-pass G-type receptor 3), NIPBL (Nipped-B-like), and FN1 (fibronectin 1). Overall, we estimate that de novo damaging variants in approximately 400 genes contribute risk in 12% of clinical cases. VIDEO ABSTRACT.