These Slc27a2 knock-out mice exhibit reduction of very long-chain acyl-CoA synthetase (VLCS) enzyme activity.
Kirby D Smith, Kennedy Krieger Institute
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by PCR or Western blot analysis. Very long-chain acyl-CoA synthetase (VLCS) enzyme activity is reduced 4-fold in liver and 9-fold in kidney. Liver microsomes and peroxisomes fractions exhibit only a residual (30% of wildtype) VLCS activity level. The very long chain fatty acid (VLCFA) beta-oxidation rate in isolated fibroblasts is reduced by approximately 40% of wildtype activity level. This mutant mouse strain may be useful in studies of X-linked adrenoleukodystrophy and/or fatty acid metabolism.
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt part of exon 3. The construct was electroporated into 129S4/SvJae derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts.
|Allele Name||targeted mutation 1, Kirby D Smith|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Slc27a2, solute carrier family 27 (fatty acid transporter), member 2|
|Strain of Origin||129S4/SvJae|
|Molecular Note||The endogenous locus was disrupted by the insertion of neo selection cassette into exon 3, deleting 69 bp of this exon. Protein was undetected in homozygous mutant mice by Western blot analysis of liver, kidney, brain, and adrenal gland homogenates.|
|Mutations Made By|| |
Ann Heinzer, Kennedy Krieger Institute
The resulting chimeric animals were crossed to 129S6/SvEvTac mice.
When using the Vlcs mice mouse strain in a publication, please cite the originating article(s) and include JAX stock #005066 in your Materials and Methods section.
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