The Journal of Experimental Medicine
Janeway's Immunobiology 7th Edition
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The Journal of Experimental Medicine, Vol 137, 1103-1107, Copyright © 1973 by The Rockefeller University Press


BRIEF DEFINITIVE REPORTS

RELATION OF CHROMOSOME 4 (LINKAGE GROUP VIII) TO MURINE LEUKEMIA VIRUS-ASSOCIATED ANTIGENS OF AKR MICE

H. Ikeda 1, E. Stockert 1, W. P. Rowe 1, E. A. Boyse 1, F. Lilly 1, H. Sato 1, S. Jacobs 1, and L. J. Old 1

1 From the Division of Immunology, Sloan-Kettering Institute for Cancer Research, New York 10021, the Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014, and the Department of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461

Genes specifying or controlling the expression of GIX (cell surface), GCSA (cell surface), and gs (internal viral) antigens are located in chromosome 4 (linkage group [LG] VIII) of the AKR mouse.

All three antigens may exhibit mendelian inheritance, mice being antigen positive or antigen negative, but each may also appear in leukemic cells of mice whose inherited genotype was antigen negative. The GIX-determining gene in LG VIII of AKR mice apparently is equivalent to Gv-1, which determines expression of the same antigen in 129 strain mice, but which in the latter strain is located in LG IX. As the estimated distance of Gv-1 from H-2 in 129 mice is considerable (37 units) further tests are now indicated to assess the possibility of pseudolinkage in this case.

The Fv-1 locus, also located in LG VIII, influences the mouse's titer of MuLV, and might thereby be thought to regulate the GIX and gs phenotypes of AKR backcross segregants. But the data indicate a discrete LG VIII locus for GIX, since expression of this antigen is mendelian and independent of infectious virus titer. Since the GIX and GCSA phenotypes of AKR backcross segregants were invariably concordant, these two antigens must be specified or controlled by closely linked genes, and the latter also is presumably independent of virus titer. The question as to what extent expression of gs antigen in the segregants is secondary to virus production is undecided.

Submitted on January 31, 1973


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