| First Author | MacDonald GP | Year | 1988 |
| Journal | Am J Hum Genet | Volume | 43 |
| Pages | A151 (Abstr.) | Mgi Jnum | J:12130 |
| Mgi Id | MGI:60383 | Citation | MacDonald GP, et al. (1988) Assignment of four human chromosome 21 genes to mouse chromosome 10: Implications for mouse models of Down Syndrome. Am J Hum Genet 43:A151 (Abstr.) |
| abstractText | Full text of Abstract: Gene Mapping and Linkage. (0601) 8.99. Assignment of Four Human Chromosome 21 Genes to Mouse Chromosome 10: Implications for Mouse Models of Down Syndrome. G.P. MacDonald1, E.R. Price1, M.-L. Chu2, R. Timpl2, R. Allore4, A. Marks4, R. Dunn4 and D.R. Cox1. 1University of California, San Francisco, 2Thomas Jefferson University, Philadelphia; 3Max-Planck Institute, Munich; 4University of Toronto, Toronto. Comparative mapping of human and mouse DNA for regions of homology between human chromosome 21 and mouse sequences has been of interest because of the possibility of developing mouse models of human trisomy 21 (Down syndrome). Mouse chromosomes 16 and 17 are known to carry sequences homologous to those on human chromosome 21. Recently, four additional genes (COL6A1, COL6A2, BPB, and CD18) have been assigned to region 21q22 of human chromosome 21. These genes code for the alpha-1 and alpha-2 chains of Type VI collagen, the Beta subunit of the glial calcium-binding protein S-100, and the shared Beta subunit of the leukocyte adhesion glycoproteins Mac-1, LFA-1, and p150,95, respectively. To assign these genes to specific mouse chromosomes, we used human cDNA probes for COL6Al, COL6A2, and CD18, and a rat cDNA probe for BPB in conjunction with a panel of seven Chinese hamster-mouse somatic cell hybrids segregating mouse chromosomes. The specific chromosome complements of the hybrids and the specific hybridization patterns of the cDNA probes to their DNAs allow us to assign all four sequences to mouse chromosome 10. These four genes provide evidence for a third region of homology between the distal long arm of human chromosome 21 and the mouse genome. Our results have implications for further efforts to construct mouse models of Down syndrome. |
