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Mutations in the Epithelial Cadherin-p120-Catenin Complex Cause Mendelian Non-Syndromic Cleft Lip with or without Cleft Palate
Journal article   Open access   Peer reviewed

Mutations in the Epithelial Cadherin-p120-Catenin Complex Cause Mendelian Non-Syndromic Cleft Lip with or without Cleft Palate

Liza L Cox, Timothy C Cox, Lina M Moreno Uribe, Ying Zhu, Chika T Richter, Nichole Nidey, Jennifer M Standley, Mei Deng, Elizabeth Blue, Jessica X Chong, …
American journal of human genetics, Vol.102(6), pp.1143-1157
06/07/2018
DOI: 10.1016/j.ajhg.2018.04.009
PMCID: PMC5992119
PMID: 29805042
url
https://doi.org/10.1016/j.ajhg.2018.04.009View
Published (Version of record) Open Access

Abstract

Non-syndromic cleft lip with or without cleft palate (NS-CL/P) is one of the most common human birth defects and is generally considered a complex trait. Despite numerous loci identified by genome-wide association studies, the effect sizes of common variants are relatively small, with much of the presumed genetic contribution remaining elusive. We report exome-sequencing results in 209 people from 72 multi-affected families with pedigree structures consistent with autosomal-dominant inheritance and variable penetrance. Herein, pathogenic variants are described in four genes encoding components of the p120-catenin complex (CTNND1, PLEKHA7, PLEKHA5) and an epithelial splicing regulator (ESRP2), in addition to the known CL/P-associated gene, CDH1, which encodes E-cadherin. The findings were also validated in a second cohort of 497 people with NS-CL/P, comprising small families and singletons with pathogenic variants in these genes identified in 14% of multi-affected families and 2% of the replication cohort of smaller families. Enriched expression of each gene/protein in human and mouse embryonic oro-palatal epithelia, demonstration of functional impact of CTNND1 and ESRP2 variants, and recapitulation of the CL/P spectrum in Ctnnd1 knockout mice support a causative role in CL/P pathogenesis. These data show that primary defects in regulators of epithelial cell adhesion are the most significant contributors to NS-CL/P identified to date and that inherited and de novo single gene variants explain a substantial proportion of NS-CL/P.
Amino Acid Sequence Epithelium - pathology Genetic Predisposition to Disease Biotinylation Epithelium - metabolism Humans Palate - pathology Infant Male Cleft Palate - genetics Mutation - genetics Catenins - genetics Syndrome Whole Exome Sequencing Cleft Lip - genetics Animals Pedigree Gene Deletion Alleles Female Mice Cadherins - genetics Infant, Newborn

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