These Pomc knock-out mice fail to exhibit opoid swim stress-induced analgesia, but exhibit naloxone-induced analgesia.
Dr. Malcolm J Low, University of Michigan Medical School
Mice homozygous for the Pomctm1Low targeted mutation are viable and fertile. Homozygous mutant mice display no overt developmental or behavioral abnormalities. The hypothalmic-pituitary-adrenal axis functions normally. Homozygotes do display significantly greater nonopioid analgesia in response to cold water swim stress compared with controls and display paradoxical naloxone-induced analgesia. Male mice show an altered growth curve during puberty resulting in increased body mass and white fat. This phenotype is present in both the homozygous mutant males and in wildtype males reared by homozygous parents. This strain is useful for looking at response to pain.
The gene targeting vector POMCX*4 encoding a truncated POMC prohormone caused by a point mutation in exon 3 and containing the phosphoglycerate kinase-neo and phosphoglycerate kinase-tk selection cassettes was constructed and electroporated into D3 embryonic stem cells. Correctly targeted ES cells were microinjected into C56BL/6 blastocysts.Per the investigator:
|Allele Name||targeted mutation 1, Malcolm J Low|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||beta-END-; betaend-; End-; POMCX*4-|
|Gene Symbol and Name||Pomc, pro-opiomelanocortin-alpha|
|Strain of Origin||129S2/SvPas|
|General Note||Additional reference J:65685 identifies the ES cell line origin as 129S2/SvEv. It is more likely that the mice used in this additional reference were derived from the targeted D3 ES cells (129S2/SvPas) first generated in J:78759 and implanted in mice in J:47711.|
|Molecular Note||A PGK-neomycin based targeting vector was used to introduce a premature start codon into exon 3, resulting in the truncation of the translated protein. In situ hybridization on homozygous mutant animals demonstrates that the truncation event had no effect on the distribution or level of transcript. Immunoreactivity demonstrated that Homozygous mutant mice had no detectable beta endorphin activity in the hypothalamus or pituitary|
|Mutations Made By|| |
Dr. Malcolm Low, University of Michigan Medical School
This strain may be maintained by mating homozygous siblings. Male offspring of homozygote beta-endorphin deficient parents have increased weight and white adipose tissue as adults compared to rearing by wildtype mothers. Expected coat color from breeding:Black
When using the β-endorphin deficient mouse strain in a publication, please cite the originating article(s) and include JAX stock #003191 in your Materials and Methods section.
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