Homozygous mutations of EDNRB in human have been reported to result in Waardenburg-Hirschsprung disease (WS4), while mutated heterozygotes manifested isolated Hirschsprung disease in lower penetrance. We investigated a case of WS4 together with all members of her nuclear family for the alteration of the EDNRB gene by using PCR-SSCP and direct sequencing technique. The index patient, who was born to a family with no history of Hirschsprung disease, presented total colonic aganglionosis with small bowel extension, sensorineural hearing loss and generalized cutaneous pigmentary defects. Interestingly, both irides were normally black. The study detected a homozygous missense mutation at codon 196 in exon 2 (Ser196Asn), which has not been reported. Both parents and four in six siblings harbored heterozygous mutation without any clinical manifestation. Our findings were consistent with previous observations that full spectrum of WS4 occurred to the mutate homozygotes. Moreover, the non-penetrance of heterozygotes in our pedigree, which differs from other reports, demonstrates the high pleiotropic effect of EDNRB mutations in human.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s00383-005-1553-z | DOI Listing |
BMJ Case Rep
December 2017
Department of Paediatrics, Bapuji Child Health Institute and Research Centre, Davangere, India.
We present the case of a 45-day-old child with the chief complaint of failure to pass stools for 10 days. After initial investigation, the patient was found to have Hirschsprung's disease. However, with further examination and analysis, the extremely rare diagnosis of type 4 Waardenburg syndrome was made (also known as Shah-Waardenburg syndrome or Waardenburg-Hirschsprung's disease).
View Article and Find Full Text PDFHum Mol Genet
September 2015
INSERM, U955, Equipe 6, 51 Avenue du Maréchal de Lattre de Tassigny, F-94000 Créteil, France, Université Paris-Est, UPEC, F-94000 Créteil, France, DHU Ageing-Thorax-Vessel-Blood, F-94000 Créteil, France,
SOX10 is a transcription factor with well-known functions in neural crest and oligodendrocyte development. Mutations in SOX10 were first associated with Waardenburg-Hirschsprung disease (WS4; deafness, pigmentation defects and intestinal aganglionosis). However, variable phenotypes that extend beyond the WS4 definition are now reported.
View Article and Find Full Text PDFNeurobiol Dis
August 2015
Department of Mental Retardation and Birth Defect Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Ogawahigashi, 4-1-1, Kodaira, Tokyo 187-8502, Japan. Electronic address:
Distinct classes of SOX10 mutations result in peripheral demyelinating neuropathy, central dysmyelinating leukodystrophy, Waardenburg syndrome, and Hirschsprung disease, collectively known as PCWH. Meanwhile, SOX10 haploinsufficiency caused by allelic loss-of-function mutations leads to a milder non-neurological disorder, Waardenburg-Hirschsprung disease. The cellular pathogenesis of more complex PCWH phenotypes in vivo has not been thoroughly understood.
View Article and Find Full Text PDFDev Biol
October 2013
INSERM, U955, Equipe 11, Hôpital Henri Mondor, 51 Avenue du Maréchal de Lattre de Tassigny, F-94000 Créteil, France; Université Paris Est, UMR_S955, UPEC, Créteil, F-94000 Créteil, France. Electronic address:
The SOX10 transcription factor is a characteristic marker for migratory multipotent neural crest (NC) progenitors as well as several of their differentiated derivatives. The involvement of SOX10 in Waardenburg-Hirschsprung disease (pigmentation defects, deafness and intestinal aganglionosis) and studies of mutant animal models have contributed significantly to the understanding of its function in neural crest cells (NCC) in general and in the melanocytes and enteric nervous system (ENS) in particular. Cell-based studies have further demonstrated the important roles of this transcription factor in maintaining the NC progenitor cell number and in determining glial cell fate.
View Article and Find Full Text PDFDevelopment
June 2011
Cardiovascular Research Institute, University of California, San Francisco, CA 94158-2517, USA.
Waardenburg syndromes are characterized by pigmentation and autosensory hearing defects, and mutations in genes encoding transcription factors that control neural crest specification and differentiation are often associated with Waardenburg and related disorders. For example, mutations in SOX10 result in a severe form of Waardenburg syndrome, Type IV, also known as Waardenburg-Hirschsprung disease, characterized by pigmentation and other neural crest defects, including defective innervation of the gut. SOX10 controls neural crest development through interactions with other transcription factors.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!