B6.129-Scd2^tm1Myz/J

Stock number: 006879
Product name: SCD2 KO
Research areas: Cardiovascular Research, Dermatology Research, Developmental Biology Research, Diabetes and Obesity Research, Endocrine Deficiency Research, Internal/Organ Research, Metabolism Research, Research Tools

Description

Homozygous Scd2^tm1Myz knockout mice otherwise show abnormal epidermal morphology and abnormal lipid homeostasis in the skin and liver, but display 100% neonatal lethality on this C57BL/6 background.

Detailed description

While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die within 24 hours of birth. Brain tissues from homozygous mice show no expression from the targeted gene. Homozygotes exhibit neonatal lethality with 100% penetrance on this genetic background (less penetrant on 129SvEv genetic background) likely due to severe skin permeability barrier abnormalities. Null mice also have abnormal epidermal morphology and abnormal lipid homeostasis in the skin and liver. These mutant mice may be useful in studying monounsaturated fatty acid synthesis, lipid biosynthesis and metabolism, cholesterol homeostasis, and skin disease, as well as obesity and diabetes.

Development

A targeting vector was designed to replace exons 1-6 of the targeted gene with a neomycin resistance cassette. The construct was electroporated into (129X1/SvJ x 129S1/Sv)F1-derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were microinjected into C57BL/6 blastocysts, and chimeric offspring were bred to C57BL/6 mice. Heterozygous mutants were backcrossed for at least 10 generations prior to arrival at The Jackson Laboratory.

Allele

Symbol: Scd2^tm1Myz
Name: targeted mutation 1, Makoto Miyazaki
MGI accession ID: MGI:3603451
Generation method: Targeted
Attributes: Null/Knockout
Marker symbol: Scd2
Marker name: stearoyl-Coenzyme A desaturase 2
Chromosome: 19
Strain of origin: (129X1/SvJ x 129S1/Sv)F1-Kitl⁺
Molecular note: A targeting vector was designed to replace exons 1-6 of the locus, the entire coding sequence. Expression was absent in mutant brains.