| First Author | Lovell D | Year | 1981 |
| Journal | Mouse News Lett | Volume | 64 |
| Pages | 49-50 | Mgi Jnum | J:29745 |
| Mgi Id | MGI:77347 | Citation | Lovell D, et al. (1981) A new mutant at the beige locus in mice. Mouse News Lett 64:49-50 |
| abstractText | Full text of MNL contribution: A new mutant at the beige locus in mice. In August 1974 two offspring of the F50th generation of the CBA/CaLac inbred strain were born with a grey coat, lighter coloured ears and tails instead of the expected agouti coat colour. Subsequent breeding tests indicated that the coat colour variant was inherited as an autosomal recessive gene. A separate colony has been maintained by forced heterozygosity for a further thirteen generations of inbreeding. Recently it became possible to test whether this new mutant was allelic to beige. A cross between a male C57BL/6J-bgJ homozygous for beige and a female CBA/Ca homozygous for the new mutant was made. All eleven offspring (4 males, 7 females) were like the CBA/Ca mutant. When offspring of this cross were mated together the two types of coat colour - the CBA/Ca mutant type and the C57BL/6J-bgJ type were produced. The ratio of 38:12 was close to the 3:1 ratio expected from the segregation of the gene a (determining whether the coat colour is black or agouti) in an F2 cross. No agouti animals were produced. It was concluded therefore that the coat colour mutant found in the LAC'S colony of CBA/Ca is another independent allele of beige. It is to be called bgLac and will be maintained by forced heterozygosity as the strain CBA/Ca-bgLac. The beige mutant on the C57BL/6J background is an animal model for the human Chediak-Higashi Syndrome and has pigment dilution, giant lysosomes in many tissues and decreased secretion of several lysosomal enzymes from the kidney. The new mutant allele is now being studied in conjunction with Dr. R. Archer at the LAC and Dr. Harris at the Institute of Rheumatology. Preliminary evidence indicates that the new mutant has the large granules associated with the Chediak-Higashi Syndrome and also, as with the bgJ mutant, there is no evidence of Natural Killer (NK) cells. There is now some interest in the development of animals which carry both the beige and the nude mutant. This new allele, coisogenic with CBA/Ca, might also be crossed to the congenic nude CBA/N strain to produce animals which are athymic and carry the X-linked B cell deficiency. |
