| First Author | Miller RD | Year | 1993 |
| Journal | Genomics | Volume | 16 |
| Issue | 3 | Pages | 740-4 |
| PubMed ID | 8100803 | Mgi Jnum | J:12789 |
| Mgi Id | MGI:61008 | Doi | 10.1006/geno.1993.1256 |
| Citation | Miller RD, et al. (1993) The mouse severe combined immune deficiency (scid) mutation is closely linked to the B-cell-specific developmental genes VpreB and lambda 5. Genomics 16(3):740-4 |
| abstractText | 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. |
