This strain originally was maintained segregating for Os and Ces1c, which are approximately 3 cM apart on Chr 8, such that Os and Ces1cb occurred in coupling opposite the wild-type Os allele and Ces1ca. In October 2002, it was discovered that a recombination event between Os and Ces1c had resulted in the strain's becoming fixed for Ces1ca.
Genetic Background | Generation |
---|---|
|
Allele Type | Gene Symbol | Gene Name |
---|---|---|
Radiation induced | Os | oligosyndactylism |
Marker Symbol | Marker Name | |
---|---|---|
Ces1c | carboxylesterase 1C |
This strain originally was maintained segregating for Os and Ces1c, which are approximately 3 cM apart on Chr 8, such that Os and Ces1cb occurred in coupling opposite the wild-type Os allele and Ces1ca. In October 2002, it was discovered that a recombination event between Os and Ces1c had resulted in the strain's becoming fixed for Ces1ca.
Allele Name | Os |
---|---|
Allele Type | Radiation induced |
Allele Synonym(s) | |
Gene Symbol and Name | Os, oligosyndactylism |
Gene Synonym(s) | |
Strain of Origin | (101 x C3H)F1 |
Chromosome | 8 |
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. |
Marker Synonym(s) | |
---|---|
Chromosome(s) | 8 |
When using the ROP/Le-Os Ces1ca/+ Ces1ca/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #002503 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
---|---|---|
Heterozygous or Wild-Type for Os Es1<a> |
Frozen Mouse Embryo | ROP/Le-Os Ces1c<a>/+ Ces1c<a>/J Frozen Embryos | $2595.00 |
Frozen Mouse Embryo | ROP/Le-Os Ces1c<a>/+ Ces1c<a>/J Frozen Embryos | $2595.00 |
Frozen Mouse Embryo | ROP/Le-Os Ces1c<a>/+ Ces1c<a>/J Frozen Embryos | $3373.50 |
Frozen Mouse Embryo | ROP/Le-Os Ces1c<a>/+ Ces1c<a>/J Frozen Embryos | $3373.50 |
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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