History and genealogy of theH-2K b mutants from the C57BL/6Kh colony

Melvold, Roger W.; Kohn, Henry I.; Dunn, G.

doi:10.1007/bf00621950

Cited by 36 publications

(21 citation statements)

References 9 publications

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“…Lanes: 1, bm6 spleen; 2, bm6 liver; 3, B6 spleen; 4, B6 liver. involved in the recognition and effector response against allogeneic and altered-self histocompatibility antigens (10,18,23,27). The "bg series'" mutants (bmS, bm6, bm7, bm9, bm16, bm17, bml8, bm2O) are of special interest because they constitute a group of related, repetitive, and yet independent events.…”

Section: Discussionmentioning

confidence: 99%

“…However, the delineation of structure-function relationships of these molecules is hampered by the extraordinary diversity among alleles, since subtle, functionally crucial amino acid alterations would not be conspicuous against a background of 20% amino acid diversity. As a result, spontaneous in vivo mutations of the Kb gene have emerged as a powerful model system to study discrete amino acid changes associated with altered alloreactivity and associative recognition (10,18,23,27). Mutant mice are detected by skin-graft incompatibility with individuals of the parental H-2b haplotype; with such tests, mutations of the Kb allele are observed at a frequency of approximately 2 x 10-4 per locus per gamete (10).…”

mentioning

confidence: 99%

“…The "bg series" of mutants (bmS, bm6, bm7, bm9, bml6, bml7, bml8, bm2O) are notable among the Kb variants because they represent a group of related but independently arising variants that are identical to each other with regard to all histocompatibility tests ("bg series" is an historical term for members of this group; they were originally designated bgl, bg2, bg3, etc., under the old nomenclature) (19,22,23 We have studied in detail one member of the "bg series" which arose in a C57BL/6Kh homozygous mouse and now report the cloning of the Kbm6 gene. Sequence analysis of this mutant gene indicates that it differs from the Kb gene by only two nucleotides, positioned 15 nucleotides apart, resulting in amino acid substitutions at residues 116 and 121.…”

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confidence: 99%

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Interaction between Kb and Q4 gene sequences generates the Kbm6 mutation.

Geliebter¹,

Zeff²,

Schulze³

et al. 1986

Mol. Cell. Biol.

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Genetic interaction as a mechanism for the generation of mutations is suggested by recurrent (12,39).From serological studies of the K and D antigens in laboratory and wild mouse populations it has been estimated that greater than 50 alleles of each exist, attesting to the tremendous polymorphism of these loci (11). Sequence analyses of various alleles of the K, D, and L loci indicate that loci and alleles differ equally from each other by approximately 20% over the 200 amino-terminal amino acids and by 11% on the corresponding nucleotide level (8,13,28,43). This large diversity among alleles is in sharp contrast to that observed at other genetic loci, where alleles usually differ from one another by only a few amino acids. This diversity is also remarkable with regard to the high conservation of Qa-and TL-region genes and their protein products, since limited tryptic peptide and DNA sequencing analyses indicate that alleles in these regions exhibit consid-* Corresponding author. t Present address:

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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Interaction between Kb and Q4 gene sequences generates the Kbm6 mutation.

Geliebter¹,

Zeff²,

Schulze³

et al. 1986

Mol. Cell. Biol.

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“…1B). Both (4,21). Because meiotic cell division results in a single gamete in the female, this pattern excludes twinning as the explanation for the coincidental appearance of mutations among siblings.…”

Section: Resultsmentioning

confidence: 99%

Unusual mutation clusters provide insight into class I gene conversion mechanisms.

et al. 1993

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Genetic diversity among the K and D alleles of the mouse major histocompatibility complex is generated by gene conversion among members of the class I multigene family. The majority of known class I mutants contain clusters of nucleotide changes that can be traced to linked family members. However, the details of the gene conversion mechanism are not known. The bm3 and bm23 mutations represent exceptions to the usual pattern and provide insight into intermediates generated during the gene conversion process. Both of these variants contain clusters of five nucleotide substitutions, but they differ from the classic conversion mutants in the important respect that no donor gene for either mutation could be identified in the parental genome. Nevertheless, both mutation clusters are composed of individual mutations that do exist within the parent. Therefore, they are not random and appear to be templated. Significantly, the bm3 and bm23 mutation clusters are divided into overlapping regions that match class I genes which have functioned as donor genes in other characterized gene conversion events. The unusual structure of the mutation clusters indicates an underlying gene conversion mechanism that can generate mutation clusters as a result of the interaction of three genes in a single genetic event. The unusual mutation clusters are consistent with a hypothetical gene conversion model involving extrachromosomal intermediates.

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“…Singer, Bethesda, MD. The mouse strains used in this study, their H-2 haplotypes, and the structural alterations in the H-2 molecules of the mutant mouse strains are listed in Table I ( [33][34][35][36][37].…”

Section: Methodsmentioning

confidence: 99%

Thymus dictates major histocompatibility complex (MHC) specificity and immune response gene phenotype of class II MHC-restricted T cells but not of class I MHC-restricted T cells.

Kast¹,

Waal²,

Melief³

1984

The Journal of Experimental Medicine

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Athymic H-2b nude mice received grafts from C57BL/6 (Sendai virus and H-Y antigen cytotoxic T lymphocyte [CTL] responder type), bm1 (H-2Kb mutant, Sendai CTL nonresponder type), or bm12 (H-21-A mutant, H-Y CTL nonresponder type) neonates. In observations of the CTL response to H-Y, both recipients and thymus donors were female. All types of thymus engraftment resulted in mature H-2b splenic T lymphocyte surface phenotype in nude hosts. T cell immunocompetence (as measured by major histocompatibility complex [MHC] CTL responses to allogeneic cells) was restored, and induced nonresponsiveness to the MHC determinants of the engrafted thymus in the nude host. The CTL reaction to Sendai virus in both responder type C57BL/6 and nonresponder type bm1 neonatal thymuses allowed maturation of Sendai-specific, H-2Kb-restricted CTL. For the CTL reaction to H-Y, only responder type C57BL/6 thymuses restored the CTL response, whereas this was not achieved with thymuses from nonresponder type bm12 neonatal females. Results of double thymus (B6 and bm12) engraftment excluded the possibility that this latter effect was caused by suppression. In addition, athymic bm1 mice were engrafted with thymuses from either B6 (Sendai CTL responder type) or syngeneic bm1 neonates (Sendai CTL nonresponder type). Again, both types of neonate thymuses restored T cell competence as measured by MHC/CTL responses to allogeneic cells. However, neither responder B6 nor nonresponder bm1 neonate thymus grafts allowed maturation of Sendai-specific CTL. In conclusion, the thymus dictates MHC specificity and immune response gene phenotype of T cells restricted to class II MHC molecules but not of T cells restricted to class I MHC molecules.

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History and genealogy of theH-2K b mutants from the C57BL/6Kh colony

Cited by 36 publications

References 9 publications

Interaction between Kb and Q4 gene sequences generates the Kbm6 mutation.

Interaction between Kb and Q4 gene sequences generates the Kbm6 mutation.

Unusual mutation clusters provide insight into class I gene conversion mechanisms.

Thymus dictates major histocompatibility complex (MHC) specificity and immune response gene phenotype of class II MHC-restricted T cells but not of class I MHC-restricted T cells.

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