Cytological Identification of the Chromosome Carrying the IXth Linkage Group (Including H-2) in the House Mouse

Klein, Jan

doi:10.1073/pnas.68.7.1594

Cited by 26 publications

(15 citation statements)

References 11 publications

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“…The observation that the allele T specifies an antigen on the surface of sperm is thus a needed vindication of the prediction that genes with a morphogenetic role will be found to code for components of the cell surface. It also, incidentally, supports the premise that the altered transmission ratios (13) and they may well suppress crossingover in the opposite direction; in any case the T-locus is so close to the centromere, perhaps even adjacent to the centromeric heterochromatin according to Klein (14), that even the allele T, which is not known to suppress recombination, might be expected to produce a detectable haploid effect; (b) X and Y chromosomes are thought not to undergo crossingover (12), Our results with anti-T serum are compatible with some degree of haploid influence because in cytotoxic tests considerably less than 100% of sperm from T/+ heterozygotes were susceptible to anti-T antibody, suggesting that some sperm had less or no antigen T. This interpretation is unwarranted however, as the serological system is a relatively weak one, with low antibody titers; thus there is no justification for concluding that sperm not lysed in the cytotoxic test are devoid of antigen. Furthermore, the considerations concerning the effect of crossingover on the gene content of immature sperm suggest that even where a haploid effect might be demonstrable it would be partial rather than complete.…”

Section: Discussionmentioning

confidence: 50%

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Serological Detection of a Cell-Surface Antigen Specified by the T (Brachyury) Mutant Gene in the House Mouse

Bennett

Goldberg

Dunn

et al. 1972

Proc. Natl. Acad. Sci. U.S.A.

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A cell-surface component specified by a mutant gene at the T-locus in the mouse has been detected on sperm by serological methods. The gene product thus recognized is not present on other adult cells.At present, there is in mammals no single morphogenetic event of which the mechanisms and controls are really understood. One recurrent theme common to the thinking of most embryologists has been that during the sorting out of cells, which comprises a large part of embryonic development, the surfaces of the cells must come to bear differential displays that can serve as recognition devices.Among many others, two of us (D.B., L.C.D.) have been interested for a long time in using developmental genetics as an approach to the problem of the control of differentiation. Our approach has been to use as analytical tools lethal mutants with marked morphogenetic effects on specific populations of cells in the early embryo, whose effects are therefore readily approachable descriptively. Such mutants should provide delicate ways of detecting factors or events essential to embryogenesis, since their effects may initially be restricted to the abnormality or absence of a single gene product. We have concentrated on genetic and embryological studies of mutant alleles at the complex T-locus in linkage group IX of the mouse. Our efforts and those of others (for review see refs. 1 and 2) have revealed in the region of the T-locus a well defined system of morphological mutants. The abnormalities produced by these mutants in both heterozygous and homozygous condition have led us to suspect that aberrations of the cell surface may be responsible (3). GeneticsThe T-locus is marked by a dominant mutant, T, which in heterozygotes leads to a shortened tail and in homozygotes to lethality midway through embryogenesis. Recessive alleles at the locus are identified by their interaction with T to produce taillessness. Several recessive embryonic lethal alleles of independent origin have been detected and maintained in balanced lethal tailless lines as T/t'. The lethal alleles that have so far been well studied are found by genetic test to fall into six different complementation groups designated Ty to, t9, t'2, t5ll, and tW5. Alleles of any one complementation group have similar homozygous effects on embryonic development and these are different from those of any other group in time and in detail. EmbryologyThe earliest effect of each of the six lethal T-locus alleles can be characterized, in general terms, as an interference with apparent switch points, which occur as ectodermal and primitive streak derivatives diverge along separate pathways. The embryology of the lethal homozygotes suggests an inability of particular groups of cells either to reach their normal location or to maintain their morphological positions or their viability once they have attained their destinations. An extensive discussion of the detailed morphogenetic defects seen in all the homozygous lethal T-locus mutants is not appropriate here. It will suffice to say t...

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Section: Discussionmentioning

confidence: 50%

“…Selected mice yielding good antiserum were bled from the tail 7, 10, and 14 (8) is added to each tube, and the proportion of dead (stained) sperm counted in a counting-chamber. Controls consisted of tubes in which phosphate-buffered saline was substituted for either antiserum or horse serum.…”

Section: Methodsmentioning

confidence: 99%

Serological Detection of a Cell-Surface Antigen Specified by the T (Brachyury) Mutant Gene in the House Mouse

Bennett

Goldberg

Dunn

et al. 1972

Proc. Natl. Acad. Sci. U.S.A.

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“…According to Nesbitt (1974), the banding pattern of rat chromosome 14 is very similar, if not exactly the same, to that of mouse chromosome 17 which carries the mouse MHC locus (Klein 1971;Miller et al 1972), and on these bases, she predicted the rat MHC locus on the chromosome 14. Our data fulfil this prediction and further substantiate the current notion that the chromosome banding similarity reflects the conservation of the homologous gene in different species, as have been shown by comparative gene mapping (Human Gene Mapping 5, 1979;Garver et al 1980).…”

Section: Immunoselection Of the Hybrid Clonesmentioning

confidence: 99%

“…The search for the genetic role of the MHC has thus become a subject of special interest in recent years, and the chromosomal organization of the MHC region is predicted to be highly conservative during evolution, showing striking similarities in the mouse, rat and man (Gill et al 1978). The mouse MHC (H-2) locus has been mapped on chromosome 17 by comparative analyses of likage groups and chromosome banding patterns in some translocation stocks (Klein 1971;Miller et al 1972). …”

Section: Introductionmentioning

confidence: 99%

Provisional chromosome assignment of the rat major histocompatibility complex.

Oikawa

Yoshida

Satoh

et al. 1983

The Japanese journal of genetics

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Somatic cell hybrids between an AKR mouse thymic lymphoma cell line and normal F344 rat spleen cells were isolated in order to assign the rat major histocompatibility complex (MHC) (RT1) to a specific chromosome. Six primary hybrid clones and 3 of their derivatives were examined for expression of the RT1 antigens on the cell surface by the complement-dependent cytotoxicity test and simultaneously for their karyotypes by the Hoechst 33258/quinacrine mustard double staining method. All of these hybrid clones consisted of 2 sets of mouse and 1 set of rat parental cells, with a preferential loss of rat chromosomes. A high degree of concordance was shown between the expression of the RT1 antigen and the presence or absence of rat chromosome 14 in the original 6 hybrid clones. This was confirmed in 1 spontaneous and 2 immunoselected RT1-negative segregants from RT1-positive clones. These results led us to propose that the rat MHC is located on chromosome 14.

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“…Discussion Considerable interest centers on mapping genes that code T cell receptor(s) for Ag/ L In fact finding the chromosomes that do not bear the receptor(s) is probably as significant as finding the ones that do, depending on which these turn out to be. Various theoretical and experimental considerations have suggested that in the mouse genes controlling Ag/I receptors should be found on chromosomes bearing immunoglobulin heavy chain genes and/or MHC genes, i.e., chromosomes 12 and 17, respectively (6)(7)(8)(9)(10)(11)(12)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23). Since on occasion Ag-binding T cell products have been shown to bear immunoglobulin idiotypes thought to be controlled by a combination of immunoglobulin light and heavy chains, chromosomes bearing light chain genes, i.e., chromosomes 6 and 16 (21,22), may also be implicated, although this is apparently not necessarily true (35).…”

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confidence: 99%

Use of somatic cell genetics to study chromosomes contributing to antigen plus I recognition by T cell hybridomas.

Marrack¹,

Kappler²

1983

The Journal of Experimental Medicine

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Keyhole limpet hemocyanin (KLH)/I region-specific T cell hybridomas have been prepared by fusing KLH/I-specific T cell blasts from mice with single pairs of metacentric chromosomes to the inducible, interleukin 2 (IL-2)-secreting T cell hybridoma FS6-14.13.AG2.1. T cell hybridomas with KLH/I receptors were identified by their ability to secrete IL-2 in response to KLH and the appropriate antigen-presenting cells. After cloning and subcloning, KLH/I reactivity was correlated with the presence or absence of metacentric chromosomes derived from the KLH/I-specific T cell blast parent. Hybridomas were identified that had lost all chromosomes 4 and 6 or 16 and 17 derived from their normal T cell parent, but retained the ability to respond to KLH/I. This suggested that products of genes on these chromosomes did not contribute to the specific portions of T cell Ag/I receptors. These gene products would include, of course, kappa and lambda chains and H-2. We did not obtain any T cell hybridomas that had lost both metacentric (8.12) chromosomes derived from T cells of the Robertsonian mouse strain Rb(8.12)5, so we could not draw any conclusions about the contributions of products of genes on these chromosomes. T cell hybridomas with KLH/I reactivity were found that contained only one metacentric (8.12) chromosome derived from this strain. Moreover, a T cell hybridoma was found that retained both metacentric (8.12) chromosomes from its normal T cell parent, but had lost KLH/I reactivity. These results suggested that neither two chromosomes 8 nor two chromosomes 12 were required for antigen/I reactivity in normal T cells and that antigen/I reactivity was controlled, at least in part, by genes mapping on chromosomes other than 8 or 12.

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Cytological Identification of the Chromosome Carrying the IXth Linkage Group (Including H-2) in the House Mouse

Abstract: Mus poschiavinus X M. musculus hybrids, which had seven metacentric chromosomes derived from the poschiavinus complement, were repeatedly backcrossed to M. musculus and selected for the chromosome carrying the H-2 complex. A

Cited by 26 publications

References 11 publications

Serological Detection of a Cell-Surface Antigen Specified by the T (Brachyury) Mutant Gene in the House Mouse

Serological Detection of a Cell-Surface Antigen Specified by the T (Brachyury) Mutant Gene in the House Mouse

Provisional chromosome assignment of the rat major histocompatibility complex.

Use of somatic cell genetics to study chromosomes contributing to antigen plus I recognition by T cell hybridomas.

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