Homozygous Ppard knock-out mice on this genetic background die in utero. Heterozygous mice or homozygous embryo-derived cells may be useful in applications related to epidermal/keratinocyte function and inflammatory response.
Yaacov Barak, University of Pittsburgh
Heterozygous mice are viable and fertile. All homozygous mice die in utero. Macrophages homozygous for this mutation have no transcriptional response to very low-density lipoprotein treatment. No evaluation of lacZ expression is published. The donating investigator reports homozygous mice on this background have a similar, albeit earlier, embryonic phenotype as the exon 4 deleted mutants described in other publications (Barak PNAS 2002 99:303-8, Chawla PNAS 2003 100:1268-73, and Lee Science 2003 302:453-7). Heterozygous mice or homozygous embryo-derived cells may be useful in studies of embryo development, adipocyte physiology, fat metabolism and storage, inflammation, and cancer.
A cell line (clone IIIA4) heterozygous for a loxP-deletion of exon 4 was originally generated from 129S4/SvJae-derived J1 embryonic stem (ES) cells (see Stock No. 005897). A targeting vector designed to replace the wild type exon 4 with a beta-galactosidase gene upstream of the DNA binding domain was electroporated into these cells. Resultant heterozygous cells (lacZ/-) were then injected into C57BL/6J blastocysts. Chimeric mice were backcrossed to C57BL/6 mice for approximately 7 generations.
|Allele Name||targeted mutation 2, Ronald M Evans|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Ppard, peroxisome proliferator activator receptor delta|
|Gene Synonym(s)||FAAR; NR1C2; NUC1; NUCI; NUCII; Nr1c2; PPAR-delta; PPARB; PPARdelta/beta; Peroxisome proliferator-activated receptor beta; Pparb; Pparb/d|
|Strain of Origin||129S4/SvJae|
|Molecular Note||The wild-type exon 4 is replaced with an in-frame lacZ gene upstream of the DNA binding domain. Although no evaluation of beta-galactosidase expression is published, we have been informed that beta-galactosidase expression has not been detected (personal communication).|
|Mutations Made By|| |
Ronald Evans, The Salk Inst for Biological Studies
|Please inquire about possible genotypes.|
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