Mice homozygous for this targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4+CD8- and CD4-CD8+ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
This targeted mutant strain was developed by Dr. Peter Mombaerts in the laboratory of Dr. Susumu Tonegawa at the Center for Cancer Research, Massachusetts Institute of Technology. A replacement targeting vector containing Pgk-neo was used which resulted in a 4 kb deletion encompassing most of the delta chain constant region coding sequences. This strain was generated in the laboratory of Dr. Leonard Shultz by backcrossing mice from B6.1292-Tcrdtm1Mom/J to BALB/cByJ inbred mice for a minimum of 9 generations.
|Allele Name||targeted mutation 1, Peter Mombaerts|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||C-delta-; delta-; delta0; gammadelta TCR-; TCRdelta-; TCRdelta KO|
|Gene Symbol and Name||Tcrd, T cell receptor delta chain|
|Strain of Origin||129P2/OlaHsd|
|Molecular Note||A PGK-neo cassette was used to disrupt the constant gene segment (designated C-delta). Flow cytometry showed that cells isolated from the lymphoid or epithelial organs of homozygous mice did not react with an anti-pan Tcrd mAb. Immunoprecipitation showed an absence of expression on the surface of thymocytes isolated from homozygous mutant embryos.|
|Mutations Made By|| |
Peter Mombaerts, Max Planck Research Unit for Neurogenetics