| First Author | Buchberg AM | Year | 1987 |
| Journal | Mouse News Lett | Volume | 79 |
| Pages | 62 | Mgi Jnum | J:14131 |
| Mgi Id | MGI:62306 | Citation | Buchberg AM, et al. (1987) The use of interspecific hybrid analysis to identify conserved linkage groups between mouse and man: identification of a new locus involved in murine and possibly human diseases. Mouse News Lett 79:62 |
| abstractText | Full text of MNL contribution: THE USE OF INTERSPECIFIC HYBRID ANALYSIS TO IDENTIFY CONSERVED LINKAGE GROUPS BETWEEN MOUSE AND MAN: IDENTIFICATION OF A NEW LOCUS INVOLVED IN MURINE AND POSSIBLY HUMAN DISEASES. A.M. Buchberg l, H.G. Bedigian 2, B.A. Taylor 2, E. Brownell l, J.N. Ihle l, S. Nagata 3, M.M. LeBeau 4, N.A. Jenkins l and N.G. Copeland l. 1 NCI-Frederick Cancer Research Facility, Frederick, Maryland. 2 The Jackson Laboratory, Bar Harbor, Maine. 3 University of Tokyo, Tokyo, JAPAN. 4 The University of Chicago, Chicago, Illinois. A common site of ecotropic murine leukemia virus integration, designated Evi-2 (ecotropic viral integration site-2), has been identified in BXH-2 myeloid tumors. We have determined the chromosomal location of Evi-2 as part of experiments to determine whether Evi-2 identifies a new proto-oncogene locus involved in myeloid disease. Evi-2 was mapped to mouse chromosome 11 using standard recombinant inbred strain and genetic backcross analyses. The location of Evi-2 relative to other proto-oncogene and growth factor loci located on chromosome 11 was then determined by interspecific backcross analysis. The loci included in this study were Erbb, Erba, Rel, I1-3 (interleukin-3). Csfgm (granulocyte-macrophage colony stimulating factor), and Trp53-1 (gene designation for p53). Only Erbb had previously been positioned on chromosome 11. The other loci had been mapped to chromosome 11 using somatic cell hybrids and consequently their position on chromosome 11 was not known. Several additional loci were also positioned on mouse chromosome 11 including, Erbb-2 (analogous to the Neu proto-oncogene), Csfg (granulocyte colony stimulating factor) and Cola-1 (alpha-1 Collagen). Recombination between Evi-2 and all markers analyzed was demonstrated, suggesting that Evi-2 may ultimately identify a new proto-oncogene involved in myeloid disease. The mapping study revealed a number of interesting conserved linkage groups between mouse and man. The distal half of mouse chromosome 11 is highly homologous to human chromosome 17. The loci Myh-1 (myosin heavy chain-1) and Trp53-1 are 6 cM apart on mouse chromosome 11 and are also localized to the short arm of human chromosome 17, possibly defining a conserved linkage group between man and mouse. Erba, Erbb-2, Csfg, Hox-2, Glk, Tk-1, Cola-1 and Tse-1 are located on mouse chromosome 11 and long arm of human chromosome 17. In addition, we have determined that the linkage of 11-3 and Csfgm to Csf-1 on human chromosome 5 is not conserved in mouse. We are currently determining the location of additional loci, including, Ngfr (nerve growth factor receptor) and Pdgfr (platelet-derived growth factor receptor) in mouse to determine the extent of this linkage conservation. Preliminary in situ hybridization mapping data using the mouse Evi-2 probe suggests that the human homolog of Evi-2 maps to 17ql1-21. There are three human diseases associated with rearrangements or mutations of human chromosome 17, namely, acute promyelocytic leukemia (APL), with a translocation breakpoint at band 17q21; human colorectal carcinoma, involving a pericentric deletion; and von Recklinghausen Neurofibromatosis (NF), which maps to the pericentric region. We are currently cloning the human homolog of Evi-2 to determine if Evi-2 is involved in any of these hunan diseases. Research sponsored by the National Cancer Institute. |
