These Myb knock-out mice have an embryonic lethal phenotype with embryos exhibiting defective hematopoiesis.
Dr. Michael L. Mucenski, Children's Hospital Research Fdn
Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic days 15.5. At embryonic day 13, homozygotes are normal in size and morphology, but have 10 fold lower hematocrit levels, due to anemia caused by diminished fetal hepatic erthropoiesis. In vitro examination of cells from the para-aortic, splanchnopleural (P-Sp) and aorta-gonad-mesonephros regions reveals defective hematopoiesis. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of fetal definitive hematopoiesis.
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exon 6. The construct was electroporated into 129S2/SvPas derived D3 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting chimeric male animals were crossed to C57BL/6 mice, and then backcrossed to C57BL/6 for at least 6 generations.
|Allele Name||targeted mutation 1, S Steven Potter|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Myb, myeloblastosis oncogene|
|Strain of Origin||129S2/SvPas|
|Molecular Note||The endogenous locus was disrupted by the insertion of a neomycin selection cassette into exon 6.|
|Mutations Made By|| |
Dr. Michael Mucenski, Children's Hospital Research Fdn
This strain must be maintained using heterozygotes due to homozygous embryonic lethal phenotype.
When using the c-myb- mouse strain in a publication, please cite the originating article(s) and include JAX stock #004757 in your Materials and Methods section.