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L Flaherty

Publications and source records attributed to L Flaherty.

149 records · Page 9Linked to original sources
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Inversion in the H-2 complex of t-haplotypes in mice.

Mouse t-haplotypes demonstrate strong linkage disequilibrium between t-lethal genes and specific H-2 types, presumably a result of recombination suppression between t and normal chromosomes. The observation of free recombination occurring between two complementary t-haplotypes suggested a chromosomal mismatch between t and normal chromosomes. Recent data showing the H-2 complex to be misplaced relative to two other markers, T and tf, in t-haplotypes suggested that chromosomal rearrangement in t-haplotypes might be the basis for their 'mismatch' with the normal chromosome. Here, to analyse the molecular nature of the rearrangement, we have cloned a polymorphic H-2 class I restriction fragment, which had previously been shown to map centromeric to the serologically defined H-2 complex in t-haplotypes. Genetic mapping studies show that this cloned t-DNA is homologous to the H-2 D region of wild-type chromosomes, and that the E alpha Ia gene maps telomeric to this DNA fragment in t-haplotypes, in contrast to its orientation in wild-type chromosomes. These results give molecular evidence for an inversion of H-2 in t-haplotypes, which may be at least partially responsible for recombination suppression and thus for linkage disequilibrium.

Animals↗
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Allogeneic reactivity in normal mouse serum.

Normal C57BL/6 (B6) mouse serum was tested in the direct cytotoxicity assay for specific reactivity against lipopolysaccharide (LPS)-stimulated mouse spleen cells. Selective reactivity was found in weanling and adult serum against lymphoblasts from mice that express an antigen encoded by the H-2Kk region of the major histocompatibility complex (MHC). Other strains, congenic with B6 at the MHC, did not exhibit the same alloreactivity. Serum from mice of a congenic strain being derived in our laboratory, which differs from B6 at two unlinked loci, Tla and nu, exhibited similar reactivity against the B6-H-2k LPS-stimulated lymphoblasts, implying that a competent T cell compartment is not necessary for generation of this reactivity. Such reactivities may result from environmental stimulation of the immune system, from internal immunoregulatory controls, or from some combination of these immune stimuli.

Animals↗