Recurrent SOX9 deletion campomelic dysplasia due to somatic mosaicism in the father

Am J Med Genet A. 2007 Apr 15;143A(8):866-70. doi: 10.1002/ajmg.a.31631.

Abstract

Haploinsufficiency of SOX9, a master gene in chondrogenesis and testis development, leads to the semi-lethal skeletal malformation syndrome campomelic dysplasia (CD), with or without XY sex reversal. We report on two children with CD and a phenotypically normal father, a carrier of a somatic mosaic SOX9 deletion. This is the first report of a mosaic deletion of SOX9; few familial CD cases with germline and somatic mutation mosaicism have been described. Our findings confirm the utility of aCGH and indicate that for a more accurate estimate of the recurrence risk for a completely penetrant autosomal dominant disorder, parental somatic mosaicism should be considered in healthy parents.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bone and Bones / abnormalities*
  • Chromosomes, Human, Pair 17
  • Family Health
  • Fathers
  • Female
  • Gene Deletion*
  • High Mobility Group Proteins / deficiency
  • High Mobility Group Proteins / genetics*
  • Humans
  • Infant, Newborn
  • Mosaicism*
  • Mutation
  • Nucleic Acid Hybridization
  • Penetrance
  • SOX9 Transcription Factor
  • Transcription Factors / deficiency
  • Transcription Factors / genetics*

Substances

  • High Mobility Group Proteins
  • SOX9 Transcription Factor
  • SOX9 protein, human
  • Transcription Factors