Comparative mapping of DNA markers from the familial Alzheimer disease and Down syndrome regions of human chromosome 21 to mouse chromosomes 16 and 17.
- 1 August 1988
- journal article
- research article
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences
- Vol. 85 (16), 6032-6036
- https://doi.org/10.1073/pnas.85.16.6032
Abstract
Mouse trisomy 16 has been proposed as an animal model of Down syndrome (DS), since this chromosome contains homologues of several loci from the q22 band of human chromosome 21. The recent mapping of the defect causing familial Alzheimer disease (FAD) and the locus encoding the Alzheimer amyloid beta precursor protein (APP) to human chromosome 21 has prompted a more detailed examination of the extent of conservation of this linkage group between the two species. Using anonymous DNA probes and cloned genes from human chromosome 21 in a combination of recombinant inbred and interspecific mouse backcross analyses, we have established that the linkage group shared by mouse chromosome 16 includes not only the critical DS region of human chromosome 21 but also the APP gene and FAD-linked markers. Extending from the anonymous DNA locus D21S52 to ETS2, the linkage map of six loci spans 39% recombination in man but only 6.4% recombination in the mouse. A break in synteny occurs distal to ETS2, with the homologue of the human marker D21S56 mapping to mouse chromosome 17. Conservation of the linkage relationships of markers in the FAD region suggests that the murine homologue of the FAD locus probably maps to chromosome 16 and that detailed comparison of the corresponding region in both species could facilitate identification of the primary defect in this disorder. The break in synteny between the terminal portion of human chromosome 21 and mouse chromosome 16 indicates, however, that mouse trisomy 16 may not represent a complete model of DS.This publication has 34 references indexed in Scilit:
- Report of the committee on comparative mappingCytogenetic and Genome Research, 1987
- Investigation of genetic linkage between myosin and actin genes using an interspecific mouse back-crossNature, 1985
- The alpha-globin pseudogene on mouse chromosome 17 is closely linked to H-2.The Journal of Experimental Medicine, 1984
- Lengths of chromosomal segments conserved since divergence of man and mouse.Proceedings of the National Academy of Sciences, 1984
- A technique for radiolabeling DNA restriction endonuclease fragments to high specific activityAnalytical Biochemistry, 1984
- Genetic control of the quantitative variation of erythrocytic glyoxalase-1 (GLO-1) in miceBiochemical Genetics, 1982
- Precise localization of human beta-globin gene complex on chromosome 11.Proceedings of the National Academy of Sciences, 1979
- Glyoxalase I Polymorphism in the Mouse: A New Genetic Marker Linked to H-2Science, 1977
- Partial trisomy 21Human Genetics, 1977
- Familial Down syndrome due to t(10;21) translocation: evidence that the Down phenotype is related to trisomy of a specific segment of chromosome 21.1975