Removal of this mouse colony is imminent. If live mice are needed for your studies, it is advised that they be ordered immediately. After removal, the mice will be available from a cryorecovery.
Homozygous females for this knockout mutation are subfertile, producing fewer and smaller litters than wildtype controls. Decreased numbers of oocytes are also produced in response to superovulation compared to wildtype controls. Male homozygotes are fertile and exhibit epithelial hyperplasia in the bladder wall and prostatic collecting ducts. This mutant mouse strain may be useful in studies related to discerning the physiological roles of the estrogen signaling system.
Kenneth Korach, LRDT, NIEHS, NIH
Mice that are homozygous for this targeted allele are viable, normal in size and do not display any gross physical abnormalities. Stop codons inserted into exon 3 result in the production of truncated transcripts that are unlikely to be translated into a functional protein. Immunostaining of ovary tissue derived from homozygous females fails to detect protein product. Homozygous females are subfertile, producing fewer and smaller litters than wildtype controls. Decreased numbers of oocytes are also produced in response to superovulation (6 compared to 33.7 in wildtype controls). Male homozygotes are fertile and present no marked abnormalities other than epithelial hyperplasia in the bladder wall and prostatic collecting ducts. This mutant mouse strain may be useful in studies related to discerning the physiological roles of the estrogen signaling system.
A targeting vector containing a neomycin resistance gene driven by the mouse phosphoglycerate kinase promoter was used to introduce stop codons into exon 3. The construct was introduced into 129P2/OlaHsd-derived E14TG2a embryonic stem (ES) cells (BK4 subline). Correctly targeted ES cells were injected into C57BL/6J blastocysts to obtain chimeric animals. These mice were then backcrossed to C57BL/6J for eight generations. In September 2001, the line was transferred to Taconic from the NIEHS and bred to C57BL/6NTac from which homozygotes were generated.
A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, 2 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a mixed C57BL/6J ; C57BL/6N genetic background.
|Allele Name||targeted mutation 1, University of North Carolina|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||BERKO; BERKOChapel Hill; betaERKO; beta-ERKO; Erb-; ERbeta-; ERbetaKO|
|Gene Symbol and Name||Esr2, estrogen receptor 2 (beta)|
|Strain of Origin||129P2/OlaHsd|
|General Note||ES cell line = BK4, which is derived from a subclone of E14TG2a.|
|Molecular Note||A neomycin resistance cassette was inserted into exon 3 of the gene, introducing a stop codon and resulting in premature termination of translation of the Esr2 mRNA. Immunocytochemistry of ovary from homozygous mutant females showed no detectable Esr2 protein.|
|Mutations Made By|| |
Kenneth Korach, LRDT, NIEHS, NIH
The line is maintained by breeding heterozygous females to homozygous males.
When using the ERβ KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #004745 in your Materials and Methods section.