| Literature DB >> 31285555 |
Antonia Howaldt1, Sheela Nampoothiri2, Dhanya Yesodharan2, Suhas Udayakumaran3, Pramod Subash4, Uwe Kornak5,6,7.
Abstract
Craniofrontonasal syndrome (CFNS) (OMIM #304110) is a very rare, X-linked developmental disorder characterized by facial stigmata, including hypertelorism, frontonasal dysplasia, craniosynostosis, bifid nasal tip, and digital abnormalities. CFNS is caused by mutations in the Ephrin 1 gene (EFNB1) located at Xq13.1, which encodes the transmembrane protein Ephrin B1. Interestingly, heterozygous females are more severely affected than hemizygous males. We report on four individuals from four unrelated Indian families with mild-to-severe CFNS. All patients had variable degrees of hypertelorism and nasal bridge depression, which did not correlate with changes in other tissues. Although patients 3 and 4 showed the most severe facial dysmorphism and syndactyly, there were no structural CNS changes or developmental delay. In contrast, patient 1 displayed agenesis of corpus callosum and developmental delay, although facial and finger abnormalities were milder. Patients 1, 2, and 4 showed different degrees of clefting. DNA sequencing revealed four previously undescribed heterozygous mutations in exons 1 and 2 of EFNB1. Patient 1 carried the second single amino acid deletion reported up to date. The other three affected individuals harbored frameshift mutations, leading to premature termination codons. Our findings broaden the spectrum of EFNB1 mutations and illustrate the absence of an obvious correlation between mutation type, severity, and expression of symptoms.Entities:
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Year: 2019 PMID: 31285555 DOI: 10.1038/s10038-019-0638-9
Source DB: PubMed Journal: J Hum Genet ISSN: 1434-5161 Impact factor: 3.172