B6C3Fe-Del(2Hoxd8,Hoxd9-Hoxd13)1Cx/Cx

Stock number: 006549
Product name: Ironside
Research areas: Neurobiology Research

Description

The spontaneous mutation in these mice consists of multiple deletions at the homeobox D cluster (Hoxd).

Detailed description

Heterozygous mice exhibit a visible hindlimb paralysis. A much more severe paralysis with digit abnormalities is observed in homozygous mice.

Development

This spontaneous mutation arose in a NZBWF1 hybrid at The Jackson Laboratory. Genetic markers were used to determine that the mutation originated in the NZW/LacJ parental chromosome. Mice were crossed to a B6C3FeF1/J background and maintained as a heterozygote x heterozygote or F1 x heterozygote cross before being cryopreserved as sperm in 2006.

Allele

Symbol: Del(2Hoxd8,Hoxd9-Hoxd13)1Cx
Name: deletion, Chr 2, Gregory A Cox 1
MGI accession ID: MGI:3574364
Generation method: Spontaneous
Marker symbol: Del(2Hoxd8,Hoxd9-Hoxd13)1Cx
Marker name: deletion, Chr 2, Cox 1
Chromosome: 2
Strain of origin: NZW/LacJ
Molecular note: A large noncontiguous deletion of two neighboring regions (approximately 8 kb and 43 kb) left an approximately 2 kb region containing exon 1 of the Hoxd8 gene in the locus between the deleted regions. The end result is a functional deletion of Hox8d, d9, d10, d11, d12 and d13. The flanking genes, Evx2 and Hoxd4, remained intact.