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H‐2 hemizygous mutants from a heterozygous cell line: role of mitotic recombination.
Author(s) -
Rajan T.V.,
Halay E.D.,
Potter T.A.,
Evans G.A.,
Seidman J.G.,
Margulies D.H.
Publication year - 1983
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1983.tb01620.x
Subject(s) - einstein , medicine , gerontology , library science , physics , computer science , mathematical physics
Variants that no longer express an entire H‐2 haplotype were readily isolated, by immunoselection with antisera directed against the haplotype, from an H‐2b/H‐2d heterozygous Friend leukemia cell line carrying a Robertsonian translocation of the chromosomes bearing the H‐2 genetic region. These variants can be denoted as being of the phenotype H‐2b‐ H‐2d+ or H‐2b+ H‐2d‐. Some of the H‐2b‐ H‐2d+ variants: (1) lack the restriction enzyme fragments characteristic of the missing H‐2b haplotype, as assessed by Southern blot analysis; (2) express more cell surface H‐2d antigens than wild‐type cells, as assessed by flow microfluorimetry; and (3) appear to have become homozygous for the more active H‐2d‐linked allele at the Glyoxalase I locus. These variants thus seem to have lost genetic material corresponding to the H‐2b haplotype and may have gained genetic material corresponding to the H‐2d haplotype. These results are consistent with the possibility that these variants were generated by mitotic recombination.