Mice that are homozygous null for Sparc are viable and fertile. They display decreased physical activity when handled but otherwise appear normal. Sparc transcripts and protein products are not detected in these animals. They development of cataracts and osteopenia are the predominant phenotypes. Lenticular opacity starts to develop at 1 to 2 months after birth, progressing to mature cataracts by 5-8 months of age. Intracellular vacuoles are apparent at 1-2 months, leading to a disruption of fiber cell packing. In later stages, the lens capsule ruptures and displacement of lens material into the anterior chamber is evident. At 17 weeks of age, null mice exhibit 50% less trabecular bone than that found in wild type controls. The loss is 70% at 36 weeks. Decreases in both osteoclast and osteoblast numbers are observed, the cumulative effect of which is a negative bone-balance leading to profound osteopenia.
|Allele Name||targeted mutation 1, Chin Chen Howe|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Sparc, secreted acidic cysteine rich glycoprotein|
|Strain of Origin||129S/SvEv-Gpi1c|
|Molecular Note||Two tandem neomycin resistance cassettes were inserted into exon 4. No mRNA was detected by Northern blot in testis, spleen or thymus of homozygous mice.|
|Mutations Made By|| |
Chin Howe, The Wistar Institute
This strain arose on a B6;129S background. It is maintained by the donating investigator as a homozygote on a B6;129S background.
When using the SPARC KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #003728 in your Materials and Methods section.