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A Adelmann

Publications and source records attributed to A Adelmann.

7 recordsLinked to original sources
PubMed1989

Multi-gene/allele control of Mlsb of CBA/H.

Festenstein originally described the Mls locus as a single dominant autosomal gene with four alleles which mapped in the 13th linkage group of chromosome 1. We subsequently presented evidence indicating that the mixed leukocyte reaction (MLR) stimulatory products of DBA/2 and CBA/J were controlled by two independently segregating Mls loci and that Mls of C3H was in fact a composite of three independently segregating loci. Recently, Mlsd of CBA/J was shown to be composed of Mlsa of AKR and a product on C3H, which was presumed to be Mlsc. Based on strain distributions, this product cannot be encoded by the Mlsc originally defined by Festenstein. In the present report, three Mls specificities of CBA/H (Mlsb) are defined. Based on the strain distribution, we postulate that these specificities are controlled by three loci, three alleles/locus, or by some combination of the preceding two possibilities.

Alleles↗
PubMed1988

Multigene control of Mlsc.

Festenstein originally described the Mls locus as a single dominant autosomal gene with four alleles which mapped in the 13th linkage group of chromosome 1. We subsequently presented evidence which indicated that the mixed leukocyte reaction stimulatory products of DBA/2 and CBA/J were controlled by two independently segregating Mls loci. Recently, Mlsd of CBA/J was shown to be composed of Mlsa of AKR and Mlsc of C3H. In the present report, classic segregation data is presented which indicates that Mlsc of C3H is controlled by three independently segregating loci. As defined by stimulatory patterns of numerous cell lines, we postulate the following: either one of the loci is shared with BALB.K, CE, C58, and partially with MA/MyJ, one is shared with CBA/H and CBA/J, and one is shared with BALB.K, CBA/J, and partially with CE; or the groups of shared determinants are controlled by different alleles of unique loci (or locus). In any event, Mlsc appears to be composed of at least three independently segregating loci; the number of alleles/locus is being investigated. In addition, C3H was stimulated by BALB.K (both were recently postulated to be Mlsc); this epitope was shared with CBA/J, CBA/H, AKR/Cum, Ma/MyJ, and C58/J.

Animals↗
PubMed1987

Nonresponsiveness to Mlsd in F1 hybrid mice carrying Mlsa and Mlsc genes.

Neither the biological function nor a basic understanding of the enigmatic chromosome 1-encoded Mls locus of the mouse has yet been uncovered despite extensive investigations. The present report is a continuation of our genetic analyses of the Mls locus in an attempt to better define the system. Data presented here indicate that in contrast to cells of mice expressing either the Mlsa or Mlsc allele which respond in mixed leukocyte reactions to cells expressing the Mlsd allelic products, cells from (Mlsa X Mlsc)F1-hybrid mice do not. In addition, the nonresponder phenotype appears to segregate as a single autosomal genetic system in backcross animals. These findings fail to support two recently advanced hypotheses: first, that the Mls locus is nonpolymorphic, or second, that the Mls locus controls differential expression of Ia antigenic determinants. Although the mechanism by which a (responder X responder) converts to a nonresponder remains unknown, three models involving gene complementation are discussed.

Animals↗
PubMedDate not supplied

Genetic complexity of Mls.

For almost 20 years, little new has been described for Mls or the products it encodes. In the present report, data is presented which indicate that either the number of loci or the number of alleles per locus that control Mls-like products is much larger than the two-locus model or five allele-model presently envisaged.

Alleles↗