These Tcfap2a knock-out mice exhibit embryonic lethality with multiple severe developmental defects of the face, skull, sensory organs, and cranial ganglia.
Rudolf Jaenisch, Whitehead Institute, Massachusetts Institute of Technology
Genetic Background | Generation |
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|
Allele Type | Gene Symbol | Gene Name |
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Targeted (Null/Knockout) | Tfap2a | transcription factor AP-2, alpha |
Mice homozygous for the Tcfap2atm1Jae mutation die around embryonic day 9.0-9.5 due to failure of cranial closure. These embryos also show multiple severe developmental defects of the face, skull, sensory organs, and cranial ganglia. There is increased apoptosis in the midbrain of day 9 embryos, coinciding with failure of cranial closure.
This strain was developed in the laboratory of Dr. Rudolf Jaenisch at the Massachusetts Institute of Technology. Exon 5 of the Tcfap2a gene was replaced with a vector containing the neo resistance gene. The 129-derived J1 ES cell line was used. Mice have been backcrossed to BALB/c mice.
Allele Name | targeted mutation 1, Rudolf Jaenisch |
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Allele Type | Targeted (Null/Knockout) |
Allele Synonym(s) | AP-2 - |
Gene Symbol and Name | Tfap2a, transcription factor AP-2, alpha |
Gene Synonym(s) | |
Strain of Origin | 129S4/SvJae |
Chromosome | 13 |
Molecular Note | A neomycin resistance cassette replaced a genomic fragment containing exon 5, which encodes part of the DNA binding domain of the protein. |
Mutations Made By | Rudolf Jaenisch, Whitehead Institute, Massachusetts Institute of Technology |
When maintaining a live colony, heterozygous mice may be bred to wildtype mice from the colony or to BALB/cJ inbred mice (Stock No. 000651). Homozygotes die between E9-E9.5.
When using the AP-2 - mouse strain in a publication, please cite the originating article(s) and include JAX stock #002794 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
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Heterozygous or wildtype for Tfap2a<tm1Jae> |
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