These Cyp1a2 knock-out mice exhibit perinatal death with impaired respiratory function. They are suitable for use in applications related to the study of neonatal respiratory distress syndrome.
Frank J Gonzalez, National Institutes of Health (NIH/NCI)
Most homozygous 129/Sv-Cyp1a2tm1Gonz mice die perinatally with impaired respiratory function due to lung immaturity. Amniotic fluid is not properly evacuated from the lungs at birth, and the alveoli do not fill with air. Lungs of homozygous mutant mice show lower levels of surfactant-associated protein (SAP) at birth than do wild type littermates. The penetrance of this phenotype is incomplete, as approximately 30% of homozygous mutants do survive to adulthood. Surviving animals, although they lack CYP1A2 protein, appear phenotypically normal and can reproduce.
Exon 2 of the Cyp1a2 gene was disrupted using an insertion vector containing the neo resistance gene. The strain was developed on a 129/Sv background and they are currently at N10 on this background.
|Allele Name||targeted mutation 1, Frank J Gonzalez|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Cyp1a2, cytochrome P450, family 1, subfamily a, polypeptide 2|
|Strain of Origin||129S4/SvJae|
|Molecular Note||A neomycin cassette was inserted into exon 2, which is the first coding exon. Western blot analysis on liver microsomes derived from adult homozygous mice demonstrated that no detectable protein was encoded by this allele.|
|Mutations Made By|| |
Frank Gonzalez, National Institutes of Health (NIH/NCI)
When maintaining a live colony, heterozygous mice may be bred to wildtype mice from the colony or to 129S1/SvImJ mice (Stock No. 002448) inbred mice. The donating investigator found that 70% of the homozygotes die.
When using the CYP1A2- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002909 in your Materials and Methods section.