Sleven Hannah, Welsh Seth J, Yu Jing, Churchill Mair E A, Wright Caroline F, Henderson Alex, Horvath Rita, Rankin Julia, Vogt Julie, Magee Alex, McConnell Vivienne, Green Andrew, King Mary D, Cox Helen, Armstrong Linlea, Lehman Anna, Nelson Tanya N, Williams Jonathan, Clouston Penny, Hagman James, Németh Andrea H
Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Program in Molecular Biology, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA.
Am J Hum Genet. 2017 Jan 5;100(1):138-150. doi: 10.1016/j.ajhg.2016.11.020. Epub 2016 Dec 23.
Early B cell factor 3 (EBF3) is an atypical transcription factor that is thought to influence the laminar formation of the cerebral cortex. Here, we report that de novo mutations in EBF3 cause a complex neurodevelopmental syndrome. The mutations were identified in two large-scale sequencing projects: the UK Deciphering Developmental Disorders (DDD) study and the Canadian Clinical Assessment of the Utility of Sequencing and Evaluation as a Service (CAUSES) study. The core phenotype includes moderate to severe intellectual disability, and many individuals exhibit cerebellar ataxia, subtle facial dysmorphism, strabismus, and vesicoureteric reflux, suggesting that EBF3 has a widespread developmental role. Pathogenic de novo variants identified in EBF3 include multiple loss-of-function and missense mutations. Structural modeling suggested that the missense mutations affect DNA binding. Functional analysis of mutant proteins with missense substitutions revealed reduced transcriptional activities and abilities to form heterodimers with wild-type EBF3. We conclude that EBF3, a transcription factor previously unknown to be associated with human disease, is important for brain and other organ development and warrants further investigation.
早期B细胞因子3(EBF3)是一种非典型转录因子,被认为会影响大脑皮质的分层形成。在此,我们报告EBF3的新生突变会导致一种复杂的神经发育综合征。这些突变是在两个大规模测序项目中被鉴定出来的:英国发育障碍解读(DDD)研究和加拿大测序与评估效用临床评估服务(CAUSES)研究。核心表型包括中度至重度智力残疾,许多个体还表现出小脑共济失调、轻微面部畸形、斜视和膀胱输尿管反流,这表明EBF3在广泛的发育过程中发挥作用。在EBF3中鉴定出的致病性新生变异包括多种功能丧失和错义突变。结构建模表明错义突变会影响DNA结合。对错义替代的突变蛋白进行功能分析发现转录活性降低以及与野生型EBF3形成异二聚体的能力下降。我们得出结论,EBF3是一种先前未知与人类疾病相关的转录因子,对大脑和其他器官的发育很重要,值得进一步研究。