| Literature DB >> 35034092 |
Michael S Hildebrand1,2, Samuel F Berkovic3, Timothy E Green4, Mareike Schimmel5, Susanna Schubert6, Johannes R Lemke6, Mark F Bennett4,7,8.
Abstract
Pallister-Hall syndrome, typically caused by germline or de novo variants within the GLI3 gene, has key features of hypothalamic hamartoma and polydactyly. Recently, a few similar cases have been described with bi-allelic SMO variants. We describe two siblings born to non-consanguineous unaffected parents presenting with hypothalamic hamartoma, post-axial polydactyly, microcephaly amongst other developmental anomalies. Previous clinical diagnostic exome analysis had excluded a pathogenic variant in GLI3. We performed exome sequencing re-analysis and identified bi-allelic SMO variants including a missense and synonymous variant in both affected siblings. We functionally characterised this synonymous variant showing it induces exon 8 skipping within the SMO transcript. Our results confirm bi-allelic SMO variants as an uncommon cause of Pallister-Hall syndrome and describe a novel exon-skipping mechanism, expanding the molecular architecture of this new clinico-molecular disorder.Entities:
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Year: 2022 PMID: 35034092 PMCID: PMC8904774 DOI: 10.1038/s41431-021-01023-4
Source DB: PubMed Journal: Eur J Hum Genet ISSN: 1018-4813 Impact factor: 4.246