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K R Willison

Publications and source records attributed to K R Willison.

49 records · Page 3Linked to original sources
PubMed1985

The arrangement of H-2 class I genes in mouse t haplotypes.

The t haplotypes of mouse chromosome 17 bear a number of interesting mutations and rearrangements, some of which map close to the H-2 complex. Since there are many H-2 class I genes of unknown function, we have investigated their arrangement in t haplotypes using genomic Southern blots. We present a detailed chart of the H-2w30 (tw12) complex, and compare it with the arrangement in other t haplotypes and standard mouse haplotypes. The chart shows duplications, deletions, and reshuffling of conserved and divergent regions. The two major features of the t arrangement--large deletions in the Qa and Tla regions--have analogues in some standard strains, so it is unlikely that these deletions are responsible for t-specific phenotypes. The differences between t and standard mouse strains are similar, in nature and in degree, to those between different standard strains.

Alleles↗
PubMed1984

Analysis of male sterile mutations in the mouse using haploid stage expressed cDNA probes.

A differential hybridization screening procedure has identified cDNAs which correspond to RNAs which are expressed in mouse testis and at lower levels in liver and spleen. The sensitivity of this procedure is such that approximately 0.5% of 1.4 X 10(4) cDNA clones are revealed as "testis specific". We have focused on ten cDNA clones which have been used to identify RNAs expressed in the haploid phase of spermatogenesis. Using Northern blots to analyse RNA isolated from the testes of mutant mice (Tfm/Y and Sxr/+) blocked at specific stages in spermatogenesis or RNA from sexually immature mice, 8 clones have been identified which correspond to RNAs expressed uniquely or at much higher levels in meiotic or post meiotic cells.

Animals↗
PubMed1982

Neutral glycolipid antigens as developmental markers of mouse teratocarcinoma and early embryos: an immunologic and chemical analysis.

Purified rabbit antibodies to neutral glycolipids were analyzed for their binding to mouse embryonal carcinoma cells (ECC) and preimplantation mouse embryos. Antibodies to globotetraosylceramide first bind to 2 to 4-cell embryos and reach a peak of staining intensity with morulae, whereas anti-Forssman antibodies first bind to late morulae and then, most intensely, to early blastocysts. We compared the binding of a monoclonal anti-Forssman antibody with that of rabbit anti-Forssman antibodies and show that although they react similarly with ECC, they do not do so with morulae: The monoclonal antibody stained weakly and unevenly, whereas the rabbit antiserum produced a uniformly bright immunofluorescent staining. Chemical analyses revealed that globotetraosylceramide is the most abundant glycolipid of F9 ECC and that there is poor correlation between the concentration of individual glycolipids in these cells and their reactivity with antibodies to glycolipid molecules. Interestingly, the 2 Forssman antibody-reactive glycolipids of F9 ECC differ in their mobility on TLC plates from the classical Forssman antigen extracted from sheep red blood cells. This illustrates the potential problems in extrapolating from the coincident binding properties of an anti-glycolipid antibody to the chemical structure or abundance of an antigen in different cell types.

Animals↗
PubMed1981

Expression of Forssman antigen in the post-implantation mouse embryo.

The expression of Forssman antigen on the surface of cells of post-implantation mouse embryos between 5 and 7 1/2 days old and of cells of the gonads from 10 1/2 days has been followed using the monoclonal antiserum M1/22.25. In the early post-implantation embryo a lineage-related distribution is found. The inner cell mass of the blastocyst was previously shown to be Forssman antigen positive and its derivative tissues the epiblast of the 5-day embryo and the primary embryonic endoderm are also positive. The endoderm cells remain positive both over the embryonic and extraembryonic portions of the embryo but the epiblast becomes Forssman antigen negative as it differentiates into embryonic ectoderm. The extraembryonic ectoderm which is derived from the Forssman negative trophectoderm remains negative throughout. The primordial germ cells are Forssman antigen positive from their first appearance in the germinal ridge until day 14 when they become negative but after that time it is other cells not related by direct lineage which become Forssman antigen positive. These are tentatively identified as Sertoli cells precursors as it is the Sertoli cells which are the antigen-positive population in the adult testis.

Animals↗
PubMed1978

Monoclonal antibodies as probes for differentiation and tumor-associated antigens: a Forssman specificity on teratocarcinoma stem cells.

A set of monoclonal antibodies derived by fusing P3-NS1/1-Ag4-1 myeloma cells with spleen cells from a rat immunized with mouse spleen were screened for activity against a tumor cell panel. One of these antibodies was found to react only with mouse embryonal carcinoma cells and no other tumor cell type tested, including differentiated derivatives of teratocarcinomas. In the adult mouse, this antigen is expressed by subpopulations of cells in the spleen, bone marrow, lymph node, brain, kidney and testes, although not in liver and thymus. This antigen has a species and tissue distribution consistent with that of Forssman antigen. The molecules which carry this specificity on the embryonal carcinoma cells appear to be glycolipids.

Antibodies↗
PubMed1978

Expression of a Forssman antigenic specificity in the preimplantation mouse embryo.

A monoclonal antibody recognizing a Forssman antigenic specificity has been shown to react with cells of the preimplantation mouse embryo. The antigen is believed to be carried on glycolipid molecules on teratocarcinoma stem cells. This antigen is first detected on the trophectoderm of the early blastocyst. The topography of the expression on the trophectoderm is striking and novel. The antigen is no longer found on these cells after the blastocyst has hatched from the zona pellucida in utero. Inner cell masses are antigen-positive at all times. This is the first study of the distribution of a single antigenic determinant in early mouse embryogenesis.

Animals↗
PubMed1974

Nitrogenase of Klebsiella pneumoniae. Inhibition of acetylene reduction by magnesium ion explained by the formation of an inactive dimagnesium-adenosine triphophate complex.

Acetylene-reducing activity of purified nitrogenase from Klebsiella pneumoniae was studied over a range of ATP and Mg(2+) concentrations at 15 degrees C, pH7.8. Inhibition at Mg(2+) concentrations of 2.5-30mm was due to the formation of the inactive complex, Mg(2)ATP. At higher Mg(2+) concentrations an additional inhibitory effect was observed. The results were consistent with a MgATP complex being the active substrate with an apparent K(m)(MgATP)=0.4mm.

Acetylene↗
PubMedDate not supplied

Expression of three t-complex genes, Tcp-1, D17Leh117c3, and D17Leh66, in purified murine spermatogenic cell populations.

Transmission ratio distortion (TRD) is a property of the complete t-haplotype which results in the preferential transmission of the t-haplotype chromosome from heterozygous t/+ males to the majority of the progeny. Available data suggest that in t/+ males, a dysfunction of the wild-type sperm within the female reproductive tract is responsible for the observed deviation from Mendelian segregation ratios. Genetically, Lyon has shown that multiple loci within the t-complex are required for maximum levels of TRD. These loci include multiple t-complex distorters (Tcds) which act upon a single t-complex responder (Tcr). Testis-expressed genes have been cloned which map to the same subregions of the t-complex as the Tcds and Tcr and are thus considered candidate genes for the products of these loci. To begin to understand how the products of these loci biochemically control TRD, the expression of three TRD-candidate genes (Tcp-1, D17Leh117c3, and D17Leh66) has been determined in populations of spermatocytes and differentiated spermatids purified to near homogeneity by unit gravity sedimentation. Fractions covering the entire gradient were analysed resulting in a more accurate picture of the precise timing of expression than previously reported. Transcription of all three genes was up-regulated in pachytene primary spermatocytes and persisted at stable levels through the haploid spermatid stages. Significantly, only levels of mRNA encoded by D17Leh66, the candidate gene for Tcr, increased from early round to elongating-stage spermatids. If this pattern of expression does, in fact, represent Tcr, these data provide the first direct evidence that wild-type and t-haplotype Tcr elements could be differentially expressed in haploid spermatids.

Animals↗
PubMedDate not supplied

A major rearrangement in the H-2 complex of mouse t haplotypes.

A proportion of wild mice carry a chromosome 17 of which a large part is very different from the standard mouse chromosome 17. The affected region is called the t complex, and the anomalous chromosomal types are the t haplotypes. In combination with various other chromosomes 17, t haplotypes can produce crossover suppression, taillessness, transmission distortion, male sterility and lethality early in development. The various t haplotypes also carry H-2 specificities which are different from those of other mice. This, together with the fact that the lethality genes map to both sides of H-2, suggests that the major histocompatibility complex is contained within the t complex. The lack of recombination between t haplotypes and standard chromosomes 17 may be due to large-scale rearrangements. Genetic data support this idea, in that the tufted gene, the H-2 complex and a group of H-2-related genes appear to be in inverted order in t haplotypes relative to the standard chromosome 17. The mapping of several t-lethal factors close to the H-2-related genes in t haplotypes suggests that breakpoint(s) may be found here. We have now investigated the major histocompatibility complex of t haplotypes by Southern blots using a variety of cloned DNA probes, and find a major rearrangement, specific to the t haplotypes, in the Qa-2,3 region of the complex. This involves the loss of several large homology units, probably including several class I H-2-related genes, and the creation of two possible breakpoints.

Animals↗