Souzeau Emmanuelle, Siggs Owen M, Zhou Tiger, Galanopoulos Anna, Hodson Trevor, Taranath Deepa, Mills Richard A, Landers John, Pater John, Smith James E, Elder James E, Rait Julian L, Giles Paul, Phakey Vivek, Staffieri Sandra E, Kearns Lisa S, Dubowsky Andrew, Mackey David A, Hewitt Alex W, Ruddle Jonathan B, Burdon Kathryn P, Craig Jamie E
Department of Ophthalmology, Flinders University, Flinders Medical Centre, Adelaide, SA, Australia.
South Australian Institute of Ophthalmology, Royal Adelaide Hospital, Adelaide, SA, Australia.
Eur J Hum Genet. 2017 Jun;25(7):839-847. doi: 10.1038/ejhg.2017.59. Epub 2017 May 17.
Variation in FOXC1 and PITX2 is associated with Axenfeld-Rieger syndrome, characterised by structural defects of the anterior chamber of the eye and a range of systemic features. Approximately half of all affected individuals will develop glaucoma, but the age at diagnosis and the phenotypic spectrum have not been well defined. As phenotypic heterogeneity is common, we aimed to delineate the age-related penetrance and the full phenotypic spectrum of glaucoma in FOXC1 or PITX2 carriers recruited through a national disease registry. All coding exons of FOXC1 and PITX2 were directly sequenced and multiplex ligation-dependent probe amplification was performed to detect copy number variation. The cohort included 53 individuals from 24 families with disease-associated FOXC1 or PITX2 variants, including one individual diagnosed with primary congenital glaucoma and five with primary open-angle glaucoma. The overall prevalence of glaucoma was 58.5% and was similar for both genes (53.3% for FOXC1 vs 60.9% for PITX2, P=0.59), however, the median age at glaucoma diagnosis was significantly lower in FOXC1 (6.0±13.0 years) compared with PITX2 carriers (18.0±10.6 years, P=0.04). The penetrance at 10 years old was significantly lower in PITX2 than FOXC1 carriers (13.0% vs 42.9%, P=0.03) but became comparable at 25 years old (71.4% vs 57.7%, P=0.38). These findings have important implications for the genetic counselling of families affected by Axenfeld-Rieger syndrome, and also suggest that FOXC1 and PITX2 contribute to the genetic architecture of primary glaucoma subtypes.
FOXC1和PITX2的变异与Axenfeld-Rieger综合征相关,该综合征的特征是眼前房结构缺陷及一系列全身特征。所有受影响个体中约有一半会发展为青光眼,但诊断年龄和表型谱尚未明确界定。由于表型异质性很常见,我们旨在通过国家疾病登记处招募的FOXC1或PITX2携带者中,描绘青光眼与年龄相关的外显率及完整表型谱。对FOXC1和PITX2的所有编码外显子进行直接测序,并进行多重连接依赖探针扩增以检测拷贝数变异。该队列包括来自24个家庭的53名携带与疾病相关的FOXC1或PITX2变异的个体,其中1人被诊断为原发性先天性青光眼,5人被诊断为原发性开角型青光眼。青光眼的总体患病率为58.5%,两个基因相似(FOXC1为53.3%,PITX2为60.9%,P = 0.59),然而,与PITX2携带者(18.0±10.6岁,P = 0.04)相比,FOXC1携带者青光眼诊断的中位年龄显著更低(6.0±13.0岁)。PITX2携带者10岁时的外显率显著低于FOXC1携带者(13.0%对42.9%,P = 0.03),但在25岁时变得相当(71.4%对57.7%,P = 0.38)。这些发现对受Axenfeld-Rieger综合征影响的家庭的遗传咨询具有重要意义,也表明FOXC1和PITX2对原发性青光眼亚型的遗传结构有影响。