CBA/J-Pepd^dal/GrsrJ

Stock number: 003398
Product name: dark-like
Research areas: Dermatology Research, Developmental Biology Research, Internal/Organ Research, Reproductive Biology Research

Description

These mice carry a spontaneous mutation at the Pepd locus characterized by a darkened coat color, smaller size, gonad abnormalities, and dark staining urine.

Detailed description

Dark-like dal is a recessive mutation causing a darkened coat color, smaller size, gonad abnormalities, and dark staining urine. dal maps to Chromosome 7 and a previously described mutation named dark da maps to the same chromosomal region. Dark-like may be a remutation to dark da.However a test for allelism is not possible because dark is thought to be extinct. Mice homozygous for the dal mutation are easily recognized by 14 days of age by their darkened coats and smaller size. Some homozygotes appear, both phenotypically and pathologically (dense bones), to have skeletal abnormalities however X-rays appear normal. At 7 months of age females had no follicles and many corpora lutea and males mild testicular degeneration with increased Leydig cells. Serum assays for Albumin, BUN, Creatine, Bilirubin, and iron showed no significant differences from controls.

Development

dal arose spontaneously in 1981 in the CBA/J colony of Dr. Eva Eicher at The Jackson Laboratory. The CBA/J colony was then at F182. This strain has been maintained via sibling mating and in 2004 reached F182+F72. Embryos were generated for cryopreservation using F182+52+ homozygous males bred with CBA/J females.

Allele

Symbol: Pepd^dal
Name: dark-like
MGI accession ID: MGI:2683249
Generation method: Spontaneous
Attributes: Hypomorph
Marker symbol: Pepd
Marker name: peptidase D
Chromosome: 7
Strain of origin: CBA/J
Molecular note: This spontaneous mutation is a 4 base pair deletion of ACTG in exon 14 that is predicted to cause a frameshift after amino acid 409 and replace the 84 carboxy terminal amino acids with 45 novel amino acids. QPCR shows a 42% decrease in expression in homozygous embryonic hearts and prolidase activity is reduced to undetectable levels in adult liver, E15.5 and adult heart, and adult red blood cells.