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Radiation induced Allele Detail
Symbol: Os
Name: oligosyndactylism; Os
MGI ID: MGI:1857646
Gene: Os  Location: unknown  Genetic Position: Chr8, Syntenic

Show the 1 phenotype image(s) involving this allele.

Strain of Origin:  (101 x C3H)F1
Allele Type:    Radiation induced
Mutation:    Inversion
  Os involves 152 genes/genome features (Anapc10, Hhip, Gm5909 ...) View all
Mutation detailsThe 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. (J:81567, J:95333)
Inheritance:    Semidominant
View phenotypes and curated references for all genotypes (concatenated display).
In Mice Carrying this Mutation: 1 assay results
In Structures Affected by this Mutation: 15 anatomical structures
Find Mice (IMSR)
Mouse strains and cell lines available from the International Mouse Strain Resource (IMSR)
Carrying this Mutation:  Mouse Strains: 10 strains available      Cell Lines: 0 lines available
Carrying any Os Mutation:  9 strains or lines available
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).
Original:  J:13049 Gruneberg H, Genetical studies on the skeleton of the mouse. XVIII. Three genes for syndactylism. J Genet. 1956;54:113-145
All:  28 reference(s)

Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
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MGI 6.16
The Jackson Laboratory