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上皮钙黏蛋白基因中的罕见变异是单纯性唇裂伴或不伴腭裂遗传病因的基础。

Rare Variants in the Epithelial Cadherin Gene Underlying the Genetic Etiology of Nonsyndromic Cleft Lip with or without Cleft Palate.

作者信息

Brito Luciano Abreu, Yamamoto Guilherme Lopes, Melo Soraia, Malcher Carolina, Ferreira Simone Gomes, Figueiredo Joana, Alvizi Lucas, Kobayashi Gerson Shigeru, Naslavsky Michel Satya, Alonso Nivaldo, Felix Temis Maria, Zatz Mayana, Seruca Raquel, Passos-Bueno Maria Rita

机构信息

Centro de Pesquisa sobre o Genoma Humano e Células-Tronco, Departamento de Genética e Biologia Evolutiva, Instituto de Biociências, Universidade de São Paulo, São Paulo, Brasil.

IPATIMUP, Institute of Molecular Pathology and Immunology, University of Porto, Porto, Portugal.

出版信息

Hum Mutat. 2015 Nov;36(11):1029-33. doi: 10.1002/humu.22827. Epub 2015 Aug 3.

Abstract

Nonsyndromic orofacial cleft (NSOFC) is a complex disease of still unclear genetic etiology. To investigate the contribution of rare epithelial cadherin (CDH1) gene variants to NSOFC, we target sequenced 221 probands. Candidate variants were evaluated via in vitro, in silico, or segregation analyses. Three probably pathogenic variants (c.760G>A [p.Asp254Asn], c.1023T>G [p.Tyr341*], and c.2351G>A [p.Arg784His]) segregated according to autosomal dominant inheritance in four nonsyndromic cleft lip with or without cleft palate (NSCL/P) families (Lod score: 5.8 at θ = 0; 47% penetrance). A fourth possibly pathogenic variant (c.387+5G>A) was also found, but further functional analyses are needed (overall prevalence of CDH1 candidate variants: 2%; 15.4% among familial cases). CDH1 mutational burden was higher among probands from familial cases when compared to that of controls (P = 0.002). We concluded that CDH1 contributes to NSCL/P with mainly rare, moderately penetrant variants, and CDH1 haploinsufficiency is the likely etiological mechanism.

摘要

非综合征性口面部裂隙(NSOFC)是一种遗传病因仍不清楚的复杂疾病。为了研究罕见的上皮钙黏蛋白(CDH1)基因变异对NSOFC的影响,我们对221名先证者进行了靶向测序。通过体外、计算机模拟或分离分析对候选变异进行评估。三个可能致病的变异(c.760G>A [p.Asp254Asn]、c.1023T>G [p.Tyr341*] 和c.2351G>A [p.Arg784His])在四个非综合征性唇裂伴或不伴腭裂(NSCL/P)家系中按照常染色体显性遗传进行分离(Lod评分:θ = 0时为5.8;外显率为47%)。还发现了第四个可能致病的变异(c.387+5G>A),但需要进一步的功能分析(CDH1候选变异的总体患病率:2%;家族性病例中为15.4%)。与对照组相比,家族性病例的先证者中CDH1突变负担更高(P = 0.002)。我们得出结论,CDH1主要通过罕见的、中度外显的变异导致NSCL/P,并且CDH1单倍体不足可能是病因机制。

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