Loss of the BMP Antagonist, SMOC-1, Causes Ophthalmo-Acromelic (Waardenburg Anophthalmia) Syndrome in Humans and Mice

نویسندگان

  • Joe Rainger
  • Ellen van Beusekom
  • Jacqueline K. Ramsay
  • Lisa McKie
  • Lihadh Al-Gazali
  • Rosanna Pallotta
  • Anita Saponari
  • Peter Branney
  • Malcolm Fisher
  • Harris Morrison
  • Louise Bicknell
  • Philippe Gautier
  • Paul Perry
  • Kishan Sokhi
  • David Sexton
  • Tanya M. Bardakjian
  • Adele S. Schneider
  • Nursel Elcioglu
  • Ferda Ozkinay
  • Rainer Koenig
  • Andre Mégarbané
  • C. Nur Semerci
  • Ayesha Khan
  • Saemah Zafar
  • Raoul Hennekam
  • Sérgio B. Sousa
  • Lina Ramos
  • Livia Garavelli
  • Andrea Superti Furga
  • Anita Wischmeijer
  • Ian J. Jackson
  • Gabriele Gillessen-Kaesbach
  • Han G. Brunner
  • Dagmar Wieczorek
  • Hans van Bokhoven
  • David R. FitzPatrick
چکیده

Ophthalmo-acromelic syndrome (OAS), also known as Waardenburg Anophthalmia syndrome, is defined by the combination of eye malformations, most commonly bilateral anophthalmia, with post-axial oligosyndactyly. Homozygosity mapping and subsequent targeted mutation analysis of a locus on 14q24.2 identified homozygous mutations in SMOC1 (SPARC-related modular calcium binding 1) in eight unrelated families. Four of these mutations are nonsense, two frame-shift, and two missense. The missense mutations are both in the second Thyroglobulin Type-1 (Tg1) domain of the protein. The orthologous gene in the mouse, Smoc1, shows site- and stage-specific expression during eye, limb, craniofacial, and somite development. We also report a targeted pre-conditional gene-trap mutation of Smoc1 (Smoc1(tm1a)) that reduces mRNA to ∼10% of wild-type levels. This gene-trap results in highly penetrant hindlimb post-axial oligosyndactyly in homozygous mutant animals (Smoc1(tm1a/tm1a)). Eye malformations, most commonly coloboma, and cleft palate occur in a significant proportion of Smoc1(tm1a/tm1a) embryos and pups. Thus partial loss of Smoc-1 results in a convincing phenocopy of the human disease. SMOC-1 is one of the two mammalian paralogs of Drosophila Pentagone, an inhibitor of decapentaplegic. The orthologous gene in Xenopus laevis, Smoc-1, also functions as a Bone Morphogenic Protein (BMP) antagonist in early embryogenesis. Loss of BMP antagonism during mammalian development provides a plausible explanation for both the limb and eye phenotype in humans and mice.

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عنوان ژورنال:

دوره 7  شماره 

صفحات  -

تاریخ انتشار 2011