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A new allele of Gli3 and a new mutation, circletail (Crc), resulting from a single transgenic experiment

  1. Author:
    Rachel, R. A.
    Wellington, S. J.
    Warburton, D.
    Mason, C. A.
    Beermann, F.

  2. Author Address

    NCI, Mouse Canc Genet Program, POB B,Bldg 539,Room 234, Frederick, MD 21702 USA Columbia Univ, Coll Phys & Surg, Ctr Neurobiol & Behav, New York, NY USA Columbia Univ, Coll Phys & Surg, Dept Pathol, New York, NY USA Columbia Univ, Coll Phys & Surg, Dept Anat & Cell Biol, New York, NY USA Columbia Univ, Coll Phys & Surg, Dept Genet & Dev, New York, NY USA Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland Rachel RA NCI, Mouse Canc Genet Program, POB B,Bldg 539,Room 234, Frederick, MD 21702 USA
    1. Year: 2002
  2. Journal: Genesis
    1. 33
    2. 2
    3. Pages: 55-61
  4. Type of Article: Article
  1. Abstract:

    While generating transgenic lines, transgene-linked mutations can occur, which are caused by an insertional mutation at a given locus. More rarely, mutations unlinked to the transgene insertion site are observed. In the process of generating a mouse overexpressing the enzyme tyrosinase, we have obtained one transgenic line that appears to carry a semidominant insertional mutation at the Gli3 (extra toes) locus, characterized by polydactyly and skeletal malformations. Additionally, the transgenic line contained a second mutation, Crc (circletail), which appears to be unlinked to the transgene insertion site. Heterozygous Crc mice are incompletely penetrant for a circled-tail phenotype, while all homozygous Crc/Crc mice die at birth of a severe neural tube defect (craniorachischisis). Anatomical evidence from a Crc/Crc; Gli3/+ fetus indicates that these two genes may interact.

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