The spontaneous autosomal recessive mutation myodystrophy (myd) is a deletion in exons 5-7 of the glycotransferase gene (Large) on chromosome 8; causing a frameshift and premature stop codon before the first two catalytic domains. The history of Stock No. 018305 is described below.
The myodystrophy mutation (Largemyd) was discovered at The Jackson Laboratory in 1963 on the lethal spotting stock LS/LeJ (Stock No. 000262; which had been imported from University College, London in 1961). The first myodystrophic male was outcrossed to a C57BL/6J female. Matings of a homozygous mouse with a heterozygous mouse were carried out as often as possible (or as heterozygous pairs). The Largemyd mutation was found on chromosome 8 in close linkage with the radiation-induced oligosyndactylism mutation (Os; heterozygotes are fertile with fused toes and homozygotes die in utero). As such, a Largemyd/+ male (generation F38) was bred to an ROP inbred female harboring the Os and pintail mutations (Stock No. 000267); this allowed for maintenance/tracking of the Largemyd mutation by Os phenotype). After three sibling matings, oligosyndactylic animals (heterozygous for the Os mutation; Os/+) were crossed seven times to the +/+ members of the strain. At N7, an Os/+ mouse was again crossed to a Largemyd/+ mouse to establish the Os and Largemyd mutations in repulsion. This repulsion strain (Stock No. 000300) was subsequently maintained by breeding oligosyndactylic siblings (Os +/+ Largemyd) together. Stock No. 000300 was cryopreserved in 1981 by mating Os +/+ Largemyd males at N7F22-F27 to non Os (+ +/+ ?) females.
In 2012, heterozygous Largemyd mice without fused toes (wildtype at the Os locus) were obtained and bred together as Stock No. 018305.
