The mouse severe combined immune deficiency (scid) mutation is closely linked to the B-cell-specific developmental genes VpreB and lambda 5.
The mouse severe combined immune deficiency (scid) phenotype is due to a recessive, autosomal mutation which results in failed development of lymphocytes. An important step during normal lymphocyte development is the germline rearrangement of DNA segments to assemble functional immunoglobulin or T cell receptor genes. scid lymphocytes fail to rearrange these genes properly, resulting in the absence of mature B and T lymphocytes. This mutation was originally mapped to chromosome 16 by linkage to the immunoglobulin lambda light chain genes (Igl-1) and the coat color mutation mahoganoid. We have typed 288 progeny from backcrosses between MOLF/Ei or CAST/Ei and C.B-17-scid for the scid phenotype and nine other loci mapped to the centromeric region of MMU16. We have established a refined map of this region which places the scid gene between Prm-2 and Igl-1. In addition, no recombinations were found between scid and three other loci, VpreB, lambda 5, and D16Mit31, providing markers useful for isolating the scid gene by positional cloning.
Miller
R D
RD
Medical Biology Institute, La Jolla, California 92037.
Ozaki
J H
JH
Riblet
R
R
D000818:Animals; D001402:B-Lymphocytes / Q000166:cytology; D015139:Blotting, Southern; D002454:Cell Differentiation / Q000235:genetics; D003433:Crosses, Genetic; D005260:Female; D008040:Genetic Linkage; D051379:Mice; D016513:Mice, SCID / Q000235:genetics*; D009154:Mutation; D012150:Polymorphism, Restriction Fragment Length