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Publication : New regions of conserved synteny and linkage between human chromosome 16p12->p13 and mouse chromosomes 16 and 11

First Author  Deng Z Year  1995
Journal  Cytogenet Cell Genet Volume  68
Pages  180 (Abstr.) Mgi Jnum  J:24075
Mgi Id  MGI:71856 Citation  Deng Z, et al. (1995) New regions of conserved synteny and linkage between human chromosome 16p12->p13 and mouse chromosomes 16 and 11. Cytogenet Cell Genet 68:180 (Abstr.)
abstractText  Full text of Abstract: 8. New regions of conserved synteny and linkage between human chromosome 16p12->p13 and mouse chromosomes 16 and 11. Z. Deng,1 K. Johnson,2 B.P. Engelward,3 S. Lane,4 D.F. Callen,4 L.D. Samson,3 M.T. Davisson,2 and M.J. Siciliano1. 1Department of Molecular Genetics, University of Texas M.D. Anderson Cancer Center, Houston, TX; 2The Jackson Laboratory, Bar Hartor, ME, 3Department of Molecular and Cellular Toxicology, Harvard School of Public Health, Boston, MA; 4Department of Cytogenetics and Molecular Genetics, Women's and Children's Hospital, Adelaide, SA, Australia At the last chromosome 16 workshop, we introduced a region of conserved synteny centromeric to the PKDI locus (which has been mapped onto the mouse chromosome 17) between two loci (NOP3 and PRMl. PRM2) at human chromosome l6pl3 and the centromeric region of mouse chromosome 16. These loci and five others have now been ordered and localized within regions defined by a hybrid clone panel (Callen et al., Genomics 13:1178-1185, 1992) shown to contain decreasing regions of the p-arm of chromosome 16. The loci (and the hybrid clones reaching most distally on the p-arm that do not contain them) are NOP3 (CY196), PRM1, PRM2 and GSPT1 (CY19), MYH11 and MRP (CY 185), UMOD (CY 175), and CRYM (CY13). Probes for each of these loci which cross hybridize to identifiable mouse restriction fragments segregating in a mouse x Chinese hamster hybrid clone panel informative for mouse chromosomes enabled the chromosomal assignment of their mouse homologs. The mouse homologs of GSPTI, MYH11 and MRP also mapped to mouse chromosome 16 (as had the homologs of NOP3 and PRM1, PRM2) extending the region of conserved synteny on the human 16 to over 3 Mb. The mouse homologs of the next centromeric loci on the human 16 (UMOD and CRYM) were discordant with the mouse 16. More centromeric loci on the p-arm of human 16 had been shown to have homologs on mouse chromosome 7. However, Umod and Crym segregated concordantly only with mouse chromosome 17 and therefore displayed a new region of conserved synteny with mouse 17 between the regions shown to be homologous with mouse chromosomes 16 and 7. Four of the loci in the mouse 16 synteny region of human 16 (NOP3, PRM1, PRM2, GSPT1, and MYH11) had RFLPs between the mouse C.B-17 and CAST/Ei strains informative for the linkage analysis of the severe combined immunodeficiency (Scid) gene centromeric on the mouse 16. The mouse homologous loci of these were therefore mapped relative to Scid and each other using 74 backcross hybrids of those strains. The results indicate gene order and recombination distances (in cM) of: centromea-Nop3-13.0-Prm1, Prm2-3.0-Gsptl-8.0-Myh1l-3.0-Scid. The order of the four loci in the syntenic group being consistent with their order on human chromosome 16 (except being inverted with respect to the position of the centromere) identifies a new region of conserved linkage between man (>3 Mb) and mouse (24 cM). Results are summarized on the accompanying table. At the distal tip of the human chromosome 16 p-arm (where HBA is located and whose homolog is known to be on the mouse 11), we had identified a glycosylase gene (MGP) and shown it to also be on the mouse 11 (Engelward et al., Carcinogenesis 14:175-181, 1993). Here, in over 200 backcross mice we show no recombinants between Mgp and Hba indicating another region of conserved linkage.
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