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Conservation of autosomal gene synteny groups in mouse and man PETER. A. LALLEY*‡, JOHN D. MINNA†‡ & UTA FRANCKE§
‡NCI - VA Medical Oncology Branch, VA Hospital, Washington DC and Division of Cancer Treatment, National Cancer Institute, Washington DC 20422
*Present address: Oak Ridge National Laboratory, Oak Ridge, Tennessee 37830.
†To whom reprint requests should be addressed.
§Department of Pediatrics, University of California, San Diego, La Jolla, California 92093
WHILE genes on the X chromosome have been conserved during evolution1 little is known about the degree of conservation of autosomal synteny groups for species distantly related in evolution such as mouse and man. The mouse gene map based on sexual genetics2,3 has been expanded by analysis of interspecific somatic cell hybrids segregating mouse chromosomes, so that the genetic maps of man and mouse can be compared. The available information indicates that genes located on different arms of the same human chromosome are not syntenic in the mouse, and genes which are many map units apart (25−45 cM) in the mouse are unlikely to be syntenic in man4−6. In contrast, genes that are tightly linked (less than 1 cM apart) seem to remain syntenic during evolution5. In addition, in species closely related in evolution, such as mouse and rat,7 or man and non-human primates8, several homologous genes have been assigned to chromosomes that are apparently homologous by chromosome banding. Five genes in the mouse (Eno-1, Pgd, Pgm-2, Ak-2, Gpd-1) are syntenic9−11 and their human homologues have been assigned to human chromosome 1; all but the human homologue of Gpd-1 are regionally assigned to arm 1p (refs 4 and 12). This apparent conservation of a rather large autosomal synteny group prompted us to investigate the extent of conservation of other autosomal regions. The results have provided chromosomal assignments for seven gene loci in the mouse and evidence for synteny of four pairs of gene loci on four different human and mouse autosomes.
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