TBX1 Is Responsible for Cardiovascular Defects in Velo-Cardio-Facial/DiGeorge Syndrome

نویسندگان

  • Sandra Merscher
  • Birgit Funke
  • Jonathan A. Epstein
  • Joerg Heyer
  • Anne Puech
  • Min Min Lu
  • Ramnik J. Xavier
  • Marie B. Demay
  • Robert G. Russell
  • Stephen Factor
  • Kazuhito Tokooya
  • Bruno St. Jore
  • Melissa Lopez
  • Raj K. Pandita
  • Marie Lia
  • Danaise Carrion
  • Hui Xu
  • Hubert Schorle
  • James B. Kobler
  • Peter Scambler
  • Anthony Wynshaw-Boris
  • Arthur I. Skoultchi
  • Bernice E. Morrow
  • Raju Kucherlapati
چکیده

Velo-cardio-facial syndrome (VCFS)/DiGeorge syndrome (DGS) is a human disorder characterized by a number of phenotypic features including cardiovascular defects. Most VCFS/DGS patients are hemizygous for a 1.5-3.0 Mb region of 22q11. To investigate the etiology of this disorder, we used a cre-loxP strategy to generate mice that are hemizygous for a 1.5 Mb deletion corresponding to that on 22q11. These mice exhibit significant perinatal lethality and have conotruncal and parathyroid defects. The conotruncal defects can be partially rescued by a human BAC containing the TBX1 gene. Mice heterozygous for a null mutation in Tbx1 develop conotruncal defects. These results together with the expression patterns of Tbx1 suggest a major role for this gene in the molecular etiology of VCFS/DGS.

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Mice overexpressing genes from the 22q11 region deleted in velo-cardio-facial syndrome/DiGeorge syndrome have middle and inner ear defects.

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22q11.2 Deletion Syndrome

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عنوان ژورنال:
  • Cell

دوره 104  شماره 

صفحات  -

تاریخ انتشار 2001