Démurger Florence, Ichkou Amale, Mougou-Zerelli Soumaya, Le Merrer Martine, Goudefroye Géraldine, Delezoide Anne-Lise, Quélin Chloé, Manouvrier Sylvie, Baujat Geneviève, Fradin Mélanie, Pasquier Laurent, Megarbané André, Faivre Laurence, Baumann Clarisse, Nampoothiri Sheela, Roume Joëlle, Isidor Bertrand, Lacombe Didier, Delrue Marie-Ange, Mercier Sandra, Philip Nicole, Schaefer Elise, Holder Muriel, Krause Amanda, Laffargue Fanny, Sinico Martine, Amram Daniel, André Gwenaelle, Liquier Alain, Rossi Massimiliano, Amiel Jeanne, Giuliano Fabienne, Boute Odile, Dieux-Coeslier Anne, Jacquemont Marie-Line, Afenjar Alexandra, Van Maldergem Lionel, Lackmy-Port-Lis Marylin, Vincent-Delorme Catherine, Chauvet Marie-Liesse, Cormier-Daire Valérie, Devisme Louise, Geneviève David, Munnich Arnold, Viot Géraldine, Raoul Odile, Romana Serge, Gonzales Marie, Encha-Razavi Ferechte, Odent Sylvie, Vekemans Michel, Attie-Bitach Tania
Service de Génétique Clinique, CLAD-Ouest, Hôpital Sud, Rennes, France.
Département de Génétique, Hôpital Necker-Enfants Malades, Assistance Publique -Hôpitaux de Paris (AP-HP), Paris, France.
Eur J Hum Genet. 2015 Jan;23(1):92-102. doi: 10.1038/ejhg.2014.62. Epub 2014 Apr 16.
The phenotypic spectrum of GLI3 mutations includes autosomal dominant Greig cephalopolysyndactyly syndrome (GCPS) and Pallister-Hall syndrome (PHS). PHS was first described as a lethal condition associating hypothalamic hamartoma, postaxial or central polydactyly, anal atresia and bifid epiglottis. Typical GCPS combines polysyndactyly of hands and feet and craniofacial features. Genotype-phenotype correlations have been found both for the location and the nature of GLI3 mutations, highlighting the bifunctional nature of GLI3 during development. Here we report on the molecular and clinical study of 76 cases from 55 families with either a GLI3 mutation (49 GCPS and 21 PHS), or a large deletion encompassing the GLI3 gene (6 GCPS cases). Most of mutations are novel and consistent with the previously reported genotype-phenotype correlation. Our results also show a correlation between the location of the mutation and abnormal corpus callosum observed in some patients with GCPS. Fetal PHS observations emphasize on the possible lethality of GLI3 mutations and extend the phenotypic spectrum of malformations such as agnathia and reductional limbs defects. GLI3 expression studied by in situ hybridization during human development confirms its early expression in target tissues.
GLI3突变的表型谱包括常染色体显性遗传的Greig头多并指综合征(GCPS)和帕利斯特-霍尔综合征(PHS)。PHS最初被描述为一种致命疾病,伴有下丘脑错构瘤、轴后或中央多指(趾)畸形、肛门闭锁和会厌裂。典型的GCPS合并手足多指(趾)畸形和颅面特征。已发现GLI3突变的位置和性质与基因型-表型之间存在相关性,突出了GLI3在发育过程中的双功能性质。在此,我们报告了来自55个家庭的76例病例的分子和临床研究,这些病例要么存在GLI3突变(49例GCPS和21例PHS),要么存在包含GLI3基因的大片段缺失(6例GCPS病例)。大多数突变是新发现的,与先前报道的基因型-表型相关性一致。我们的结果还显示,在一些GCPS患者中,突变位置与胼胝体异常之间存在相关性。对胎儿PHS的观察强调了GLI3突变可能具有的致死性,并扩展了诸如无颌畸形和肢体发育不全等畸形的表型谱。通过原位杂交在人类发育过程中对GLI3表达的研究证实了其在靶组织中的早期表达。