B6;C-Ghrhr^lit Prkdc^scid/BmJ

Stock number: 010816
Product name: lit/scid
Research areas: Cancer Research, Cell Biology Research, Developmental Biology Research, Endocrine Deficiency Research, Immunology, Inflammation and Autoimmunity Research, Internal/Organ Research, Mouse/Human Gene Homologs, Reproductive Biology Research, Research Tools, Virology Research

Description

These double mutant mice are deficient in both growth hormone and IGF1.

Detailed description

B6;C-Ghrhr^litPrkdc^scid/BmJ mice are deficient in growth hormone and IGF1 and are useful for determining endocrine dependence of grafted cells and tissues (Beamer et al., 1993, Cancer Research, v53:3741; Friend et al., 2001 Growth Hormone & IGF Research, v11:84).

Development

A homozygote from the strain C57BL/6J-Ghrhr^lit (stock #000533) was bred with a C.BKa-Igh^b/Icr-Prkds^scid homozygote and the resulting offspring were intercrossed to generate a strain homozygous for Prkdc^scid and segregating for Ghrhr^lit. This strain was generated and maintained by sibling inbreeding in the laboratory of Dr. Wesley Beamer. In 2009 sperm were cryopreserved from males at generatiuon F31 that were homozygous for both the little and scid mutations. Cryorecovery using eggs from CBySmn.CB17-Prkdc/J females will re-introduce the Igh^a sequence.

Allele

Symbol: Prkdc^scid
Name: severe combined immunodeficiency
MGI accession ID: MGI:1857113
Generation method: Spontaneous
Marker symbol: Prkdc
Marker name: protein kinase, DNA activated, catalytic polypeptide
Chromosome: 16
Strain of origin: C.BKa-Igh^b/Icr
Site of expression: T and B lymphocytes.
Molecular note: A T-to-A transversion point mutation at a position corresponding to codon 4046 (codon 4095 in transcript ENSMUST00000023352.8) created a premature stop codon (p.Y4046*).

Allele

Symbol: Ghrhr^lit
Name: little
MGI accession ID: MGI:1856425
Generation method: Spontaneous
Marker symbol: Ghrhr
Marker name: growth hormone releasing hormone receptor
Chromosome: 6
Strain of origin: C57BL/6J
Molecular note: The mutation in little mice is a A-to-G transition in codon 60 that alters this residue from a aspartate to a glycine in the encoded protein (p.D60G). Reduced levels of mRNA were noted in total RNA derived from pituitary of homozygous mice, and in vitro assays demonstrated that no functional protein is made from this allele.