These Cycs knock-out mice exhibit embryonic lethality with embryos being devoid of cytochrome c.
Robert S Williams, Duke University School of Medicine
Mice homozygous for the Cycstm1Wlm targeted-mutant allele die in utero by embryonic day 10.5, but cell lines established from early Cycs-null embryos are viable under conditions that compensate for defective oxidative phosphorylation. Cells lacking cytochrome c show reduced caspase 3 activation, and are resistant to the proapoptotic effects of UV irradiation, serum withdrawal, and staurosporine. Cells lacking cytochrome c, however, do demonstrate an increased sensitivity to cell death signals triggered by tumor necrosis factor, alpha. Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
A targeting vector containing neomycin resistance and thymidine kinase genes was used to disrupt the entire gene and flanking sequences. The construct was electroporated into 129-derived KG-1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts and the resulting chimeric animals were crossed to C57BL/6 mice.
|Allele Name||targeted mutation 1, Robert Sanders Williams|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||Cyt c-|
|Gene Symbol and Name||Cycs, cytochrome c, somatic|
|Strain of Origin||129S6/SvEvTac|
|Molecular Note||A neomycin resistance cassette replaced the two protein coding exons. Immunoblot analysis did not detect endogenous protein in cells cultured from E8-E9 embryos of homozygous mutant mice.|
|Mutations Made By|| |
Robert Williams, Duke University School of Medicine
This strain originated on a B6;129 background. The donating investigator maintains this strain by mating heterozygotes.
When using the Cyt c- mouse strain in a publication, please cite the originating article(s) and include JAX stock #004264 in your Materials and Methods section.