Mice carrying the radiation-induced oligosyndactyly (Os) mutation on a C57BL/6 genetic background exhibit hyperlipidemia, but do not develop glomerulosclerosis as do mice carrying Os on the ROP/GnLe strain.
Mice carrying the radiation-induced oligosyndactyly (Os) mutation on a C57BL/6 genetic background exhibit hyperlipidemia , but do not develop glomerulosclerosis as do mice carrying Os on the ROP/GnLe strain (Stock No. 000267). Nephron number is decreased by 50% in both B6 Os/+ and ROP Os/+ mice, and a glomerular volume and labeling index are two- to threefold increased in both. Chow-fed B6.ROP Os/+ animals demonstrate glomerular hypertrophy with an increase in mesangial matrix and cellularity that is characterized by macrophage influx and increased proliferation. Hyperlipidemia in B6.ROP Os/+ mice results in increased plasma BUN compared to chow-fed B6.ROP Os/+ animals and aggravated renal pathology by further increasing glomerular matrix and glomerular hypercellularity. Glomerular transforming growth factor-beta (TGF-beta) mRNA expression is increased in B6.ROP Os/+ mice compared to controls.
The Os mutation was transferred from mice of strain ROP/Le onto the C57BL/6J background by repeated backcrossing reaching N27 in 2005.
|Allele Type||Radiation induced|
|Gene Symbol and Name||Os, oligosyndactylism|
|Strain of Origin||(101 x C3H)F1|
|General Note||Heterozygotes are affected on all four feet. Fusion usually occurs between the second and third digits and occasionally involves the fourth (J:13049). The muscles of the forearms and lower legs as well as of the feet show anomalous arrangements not necessarily correlated with the skeletal changes (J:12944). At 11 days of gestation the preaxial border of the limbs can be seen to be reduced (J:12942), and a histological examination at this time shows that there is a small amount of cellular degeneration in the preaxial part of the footplate mesoderm, leading to coalescence of the second and third digital rudiments (J:5107). Os /+ mice have a mild diabetes insipidus present at 5 weeks and increasing with age. In combination with one or more recessive modifying genes in the selected DI stock, Os/+ mice have a severe diabetes insipidus (J:12948). The cause of the diabetes is a 45% reduction in size of the kidneys with an 80% reduction in number of glomeruli. Compensatory hypertrophy of the nephrons is not sufficient to restore normal urine-concentrating ability (J:5127)(J:5128).|
|Molecular Note||The oligosyndactylism mutation is due to a chromosomal inversion that has breakpoints approximately 10 Mb apart. One breakpoint appears to reside in the Anapc10 gene, and an aberrant transcript consisting of part of Anapc10 and an unrelated sequence is expressed at low levels.|
When using the oligosyndactylism mouse strain in a publication, please cite the originating article(s) and include JAX stock #003523 in your Materials and Methods section.