B6.129P2-Prlr^tm1Cnp/J

Stock number: 003142
Product name: PRLR-
Research areas: Cancer Research, Developmental Biology Research, Endocrine Deficiency Research, Neurobiology Research, Reproductive Biology Research

Description

Homozygous female Prlr knock-out mice exhibit infertility and lack of mammary development.

Detailed description

There is complete female sterility due to abberant estrous cycles, abnormal preimplantation development of eggs, no implantation of blastocysts, lack of pseudopregnancy. Males show slightly delayed fertility. Mammary development is markedly affected. Homozygotes have no mammary development and do not lactate. Heterozygotes are unable to lactate after the first pregnancies, but attain some degree of lactation as they age or after multiple pregnancies. Serum prolactin levels are increased 60 - 100 fold in both males and females. Maternal behavior is diminished in pimiparous and nulliparous animals. Bone remodelling is decreased in homozygote mutants.

Development

Exon 5 was replaced with the neomycin resistance gene driven by the thymidine kinase promotor. The truncated mRNA, if produced, would encode a protein of only 44 amino acids, unable to bind the hormone and produce any biological action. The targeting construct was electroporated into 129P2/OlaHsd-derived E14.1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts. The resulting chimeric animals were bred to crossed to C57BL/6 and offspring were backcrossed to C57BL/6 for at least 10 generations.

Allele

Symbol: Prlr^tm1Cnp
Name: targeted mutation 1, Paul A Kelly
MGI accession ID: MGI:1888377
Generation method: Targeted
Attributes: Null/Knockout
Marker symbol: Prlr
Marker name: prolactin receptor
Chromosome: 15
Strain of origin: 129P2/OlaHsd
Molecular note: A neomycin cassette was inserted into exon 5, creating an in-frame stop codon. Northern, Western, and binding data all demonstrate the lack of a functional receptor in homozygous mutant animals.