Homozygous Cbx2tm1Cim (M33-) mice show greatly retarded growth, homeotic transformations of the axial skeleton, sternal and limb malformations and a failure to expand in vitro of several cell types including lymphocytes and fibroblasts. In addition, mutant mice show an aggravation of the skeletal malformations when treated to retinoic acid at embryonic day 7.5. Mutant mice develop to term and appear normal, however, most of the M33 mutant mice (90%) die within 4 weeks and the life span does not exceed 6 weeks.
The first 4 exons were replaced via homologous recombination with a floxed neomycin resistance cassette in reverse orientation. This was done in E14 ES cells, derived from 129P2/HsdOla, and ES cells were injected into BALB/c blastocysts. Germ-line transmission was obtained after a backcross between chimeric males and BALB/c females. The strain was maintained by heterozygous matings for more than 2 years. It was imported into The Jackson Laboratory from Dr. Malek Djabali in 1999 and bred to BALB/cByJ then C57BL/6JEi before being backcrossed onto DBA/2J for 9 generations.
|Allele Name||targeted mutation 1, Centre d'Immunologie de Marseille Luminy|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||M33 -|
|Gene Symbol and Name||Cbx2, chromobox 2|
|Strain of Origin||129P2/OlaHsd|
|Molecular Note||A neomycin resistance cassette replaced exons 1-4. RT-PCR analysis confirmed the absence of the transcript in homozygous mice.|
|Mutations Made By|| |
Malek Djabali, Universite Paul Sabatier - Toulouse III