Comparative mapping of DNA markers from the familial Alzheimer disease and Down syndrome regions of human chromosome 21 to mouse chromosomes 16 and 17

Journal Article · Mon Aug 01 00:00:00 EDT 1988 · Proceedings of the National Academy of Sciences of the United States of America; (USA)

DOI:https://doi.org/10.1073/pnas.85.16.6032· OSTI ID:5363125

Cheng, S V; Nadeau, J H; Tanzi, R E; Watkins, P C; Jagadesh, J; Taylor, B A; Haines, J L; Sacchi, N; Gusella, J F ^[1]

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1. Harvard Medical School, Boston, MA (USA)

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, the authors 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.

• OSTI ID: 5363125
• Journal Information: Proceedings of the National Academy of Sciences of the United States of America; (USA), Journal Name: Proceedings of the National Academy of Sciences of the United States of America; (USA) Vol. 85:16; ISSN 0027-8424; ISSN PNASA
• Country of Publication: United States
• Language: English

Related Subjects

550401* -- Genetics-- Tracer Techniques
59 BASIC BIOLOGICAL SCIENCES
ANIMALS
BIOLOGICAL MARKERS
CHROMOSOMES
CLONING
DISEASES
DNA HYBRIDIZATION
DNA-CLONING
ENZYMES
GENES
GENETIC MAPPING
GROWTH FACTORS
HEREDITARY DISEASES
HETEROCHROMOSOMES
HUMAN CHROMOSOME 16
HUMAN CHROMOSOME 21
HYBRIDIZATION
INTERFERON
LYMPHOKINES
MAMMALS
MAPPING
MICE
MITOGENS
NERVOUS SYSTEM DISEASES
ONCOGENES
ORGANIC COMPOUNDS
OXIDOREDUCTASES
PROTEINS
RODENTS
SUPEROXIDE DISMUTASE
VERTEBRATES