The Mutational Spectrum of the Sonic Hedgehog Gene in Holoprosencephaly: SHH Mutations Cause a Significant Proportion of Autosomal Dominant Holoprosencephaly

Luisa Nanni(University of Pennsylvania), Jeffrey E. Ming(Philadelphia University), Maureen Bocian(University of California, Irvine Medical Center), Kathryn A. Steinhaus(University of California, Irvine Medical Center), Diana W. Bianchi(Tufts University), Christine de Die‐Smulders(Maastricht University Medical Centre), Aldo Giannotti(Bambino Gesù Children's Hospital), K Imaizumi(Kanagawa Children's Medical Center), Kenneth Lyons Jones(University of California, San Diego), Miguel Del Campo(University of California, San Diego), R. A. Martin(St. Christopher's Hospital for Children), P. Meinecke(Altonaer Kinderkrankenhaus), Mary Ella Pierpont(University of Minnesota), Nathaniel H. Robin(Case Western Reserve University), I.D. Young(Nottingham City Hospital), Erich Roessler(National Institutes of Health), Maximilian Muenke(National Human Genome Research Institute)
Human Molecular Genetics
December 1, 1999
Cited by 360Open Access
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Abstract

Holoprosencephaly (HPE) is a common developmental anomaly of the human forebrain and midface where the cerebral hemispheres fail to separate into distinct left and right halves. We have previously reported haploinsufficiency for Sonic Hedgehog ( SHH ) as a cause for HPE. We have now performed mutational analysis of the complete coding region and intron-exon junctions of the SHH gene in 344 unrelated affected individuals. Herein, we describe 13 additional unrelated affected individuals with SHH mutations, including nonsense and missense mutations, deletions and an insertion. These mutations occur throughout the extent of the gene. No specific genotype-phenotype association is evident based on the correlation of the type or position of the mutations. In conjunction with our previous studies, we have identified a total of 23 mutations in 344 unrelated cases of HPE. They account for 14 cases of familial HPE and nine cases of sporadic HPE. Mutations in SHH were detected in 10 of 27 (37%) families showing autosomal dominant transmission of the HPE spectrum, based on structural anomalies. Interestingly, three of the patients with an SHH mutation also had abnormalities in another gene that is expressed during forebrain development. We suggest that the interactions of multiple gene products and/or environmental elements may determine the final phenotypic outcome for a given individual and that variations among these factors may cause the wide variability in the clinical features seen in HPE.


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