Genetic polymorphism of IgG in the mink. III. Instability of expression and the problem of the genetic control of C gamma-allotypes.

Quantitative expression of C gamma-allotype H4 of mink immunoglobulins was studied by enzyme-linked immunosorbent assay. The results presented suggest that production of H4 is under specific regulation. the concentration of H4 varies three orders of magnitude (10-10,000 micrograms/ml) from one mink to another. Fifteen percent of the sera of normal minks have the low H4 concentration, undetectable by the standard procedure of double immunodiffusion routinely used to test mink IgG allotypes. However, expression of these 'minor' allotypes may be significantly enhanced by hyperimmunization. Instability of this kind seems to be the main cause of earlier described deviations from Mendelian inheritance of C gamma-allotypes H2, H3 and H4.

Genetic polymorphism of IgG in the mink. IV. Identification and genetic control of L3 allotype of the light chains.

A new allotype of the mink light chains, designated L3, was identified. This allotype is inherited as a Mendelian character at a frequency of 0.46 in the mink population. Data were obtained indicating that L3 is independent of the C gamma-heavy chain allotypes of mink immunoglobulins. The gene L3 is closely linked to a gene encoding L1, another light chain allotype. Alloantigens L1 and L3 are presumably markers of the light chains of two different subtypes. In contrast to L1, which occurs in many mammalian species, L3 is species-specific, i.e., it is a case of light chain polymorphism representative of the whole mink species.

Genetic polymorphism of IgG in mink. I. Identification of 8 allotypes.

By means of intraspecific immunization of domestic mink (Mustela vison Schr.), 8, in all probability, complex IgG allotypes were detected in their sera. Based on the results of analysis of the preparations of the IgG heavy (H) and light (L) chains, as well as proteolytic IgG fragments, we assigned the allotypes detected to three groups: (1) marker of the L chain, L1; (2) allotypes of the C region of gamma-chains (H2, H3, H4, H6, and H8) and conformational allotype H7; (3) conformational allotype 5 with unknown location on the chains.

Genetic polymorphism of IgG in mink. II. A genetic analysis of allotypes.

Population distribution and inheritance pattern were analyzed in mink IgG allotypes: L1 (L chains), H2, H3, H4, H6, H7, and H8 (the constant region of the H chains, i.e. C gamma-allotypes) and conformational allotype 5 with unknown chain localization. Contrary to expectation, neither allelism, nor close linkage were demonstrated for these allotypes. The major feature of the inheritance of H2, H3, and H4 C gamma-allotypes, as well as allotype 5, was significant excess of negative (without these allotypes) progeny in the F1 generation from monohybrid cross. The explanation offered for this departure of the C gamma-allotypes from normal Mendelian genetics suggests widespread latencies of their expression in mink.

Spontaneous and induced activation of genes affecting the phenotypic expression of glucose 6-phosphate dehydrogenase in Daphnia pulex : 3. Occurrence frequencies of the alternative electrophoretic variants of G6PD in a natural population.

Evidence has previously been presented on the occurrence spontaneous variations in the electrophoretic mobility (EM) of glucose-6-phosphate dehydrogenase (G6PD E.C. 1.1.1.49) in laboratory clones of parthenogenetically reproducing Daphnia (Ruvinsky et al. 1983). The present study is concerned with a natural population of Daphnia living under the extreme conditions of shallow, dessicating pond. The number of individuals having the slow (S) variant of the EM of G6PD increased sharply during their 1.5 month life span. This increase is suggested to result from alternational variability related to activation of latent genetic material.

Mechanisms involved in the spontaneous occurrence of diploid-triploid chimerism in the mink (Mustela vison) and chicken (Gallus domesticus).

Diploid-triploid chimeras have been observed both in man and in a number of laboratory and livestock animals. The mechanism(s) of their origin remains enigmatic. One approach is to calculate for each proposed mechanism the expected frequencies of zygotes bearing different gonosomic complements in the two cell lines. Observed samples are then compared with the expectations. The mechanisms that have been considered include: (1) fertilization of a blastomere, (2) absorption of the second polar body into a blastomere, (3) fertilization of the first polar body, (4) independent fertilization of both nuclei in binucleated oocytes, (5) fertilization of the second polar body as well as the egg, and (6) fusion of two eggs. The sample of minks comprised three preimplantation embryos, nine postimplantation embryos, and three neonatal pups, with gonosomic complements of 7 XX/XXX, 3 XX/XXY, 4XY/XXY, and 1 XY/XYY; the chicks comprised 13 embryos at 1 day of incubation, 1 embryo at 4 days, and one adult bird, with gonosomic complements of 5 ZZ/ZZZ, 1 ZZ/ZZW, 1 ZW/ZZZ, 3 ZW/ZZW, and 5 ZW/ZWW. If it is assumed that within each species all, or most, of the 2n/3n chimeras arise from the same mechanism, then the occurrence of a type that has an expected frequency of zero for a given proposed mechanism effectively eliminates that mechanism as a source. All of the chicks could have resulted from only one mechanism, viz., independent fertilization of both nuclei in binucleated oocytes. The sample of minks could have resulted from the same mechanism or from fertilization of a blastomere of a two-cell, 2n embryo.

Effect of hydrocortisone on the phenotypic expression and inheritance of the Fused gene in mice.

This study was undertaken to examine the effects of hydrocortisone injected into male mice on the phenotypic expression and inheritance of the Fused (Fu) gene in their offspring. Data were obtained indicating that there is a hydrocortisone-susceptible period during spermatogenesis. Hydrocortisone injections of males during this period resulted in a statistically significant decrease in the proportion of phenotypically Fu offspring. Genetic analysis with the use of the closely linked recessive marker tufted (tf) demonstrated that the deficit of phenotypically Fu individuals among offspring is not caused by the differential death of gametes, zygotes or embryos. According to genetic data, this deficit is due to a decrease in the penetrance of the Fu gene and partly to its inherited inactivation. The possible mechanisms of the observed phenomenon are discussed.

Inherited activation-inactivation of the star gene in foxes: its bearing on the problem of domestication.

A frequency of more than 10(-2) of the de novo appearance of piebald spotting (star) was established in silver-black foxes selected for domestic behavior. The star phenotype is determined by the autosomal semidominant gene S. Ten genealogical groups of foxes, in which star arose independently, were analyzed. Of these, the star character is determined by S alleles in at least seven groups. The S gene is located in a linkage group other than the earlier described W (Georgian white) locus. The star gene is incompletely penetrant, but its penetrance is significantly higher in offspring from tame mothers than from aggressive ones, or when S is received from a heterozygous vixen (Ss). There was a notable shortage of homozygous (SS) offspring from Ss X Ss crosses, which cannot be adequately explained by selective embryonic mortality, differential zygotic and gametic death, or transgression of homozygous and heterozygous phenotypes. Some foxes, proven carriers of a homozygous (Ss) genotype, showed the phenotype and mode of inheritance characteristic of heterozygotes (Ss). Presumably, the mechanism responsible of these observations is a heritable functional activation-inactivation of the star gene. Some implications of this concept in terms of destabilizing selection are discussed.

Inheritance of alternative states of the fused gene in mice.

The genetics of the fused (Fu) gene in the house mouse, Mus musculus, was studied by use of the closely linked recessive marker, tufted (tf). Evidence was obtained indicating that Fu passes from a phenotypically active state to inactive: Fu in equilibrium with [Fu]. These alternative states may be genetically transmitted. It is suggested that the activation of a "dormant" Fu gene may underlie this passage.

Immunogenetic study on the polymorphism of serum alpha2-lipoproteins in mink. II. Identification of allotypes Lpm-7 and Lpm-8 and genetic control of seven markers of the Lpm system.

By means of alloimmunization of mink, two new antigens, Lpm-7 and Lpm-8, were detected in their sera. Lpm-7 and Lpm-8 allospecificities were referred to a very high density alpha2-lipoprotein (Lpm) by the following criteria: histochemical tests, immunoelectrophoresis, preparative ultracentrifugation, and coalescence of alloprecipitates with heteroprecipitates in double diffusion tests. Genetic analysis indicated that Lpm-7 and Lpm-8, together with the earlier described Lpm-1, Lpm-2, Lpm-3, Lpm-4, and Lpm-5, share a common immunogenetic system. Polymorphism for the seven markers is conditioned by the genetic units Lpm8, Lpm4, Lpm4,8, Lpm4,7, Lpm3,4,8, Lpm1,8, Lpm1,2,7, and Lpm2,4,5,7, which behave as alleles. Of these units, the latter six are probably haploid sets of closely linked genes.

Immunogenetic study on the polymorphism of serum alpha2-lipoproteins in mink. I. Identification and genetic control of five Lpm allotypes.

Five allotypes, Lpm 1, Lpm 2, Lpm 3, Lpm 4, and Lpm 5, were detected by isoimmunization in mink sera. Immunoelectrophoresis, preparative ultracentrifugation, and histochemical tests for lipids and esterase permitted reference of these alloantigenic markers to a very high density alpha2-lipoprotein. Based on population analysis and breeding tests, five genetic units are postulated: Lpm1, Lpm4, Lpm3,4, Lpm1,2, and Lpm2,4,5. These units determine the polymorphism of the Lpm system and behave as Mendelian alleles.

Genetics of the W locus in foxes and expression of its lethal effects.

The Georgian white mutation for coat color in foxes is inherited as a partially dominant character. It is allelic to the previously observed white-faced and platinum mutations. It was established that large litter size in Georgian white females and long daylight during pregnancy promote embryonic viability in homozygotes for this mutation. As a result, in offspring segregation patterns for coat color the proportion of homozygotes increases and that of heterozygotes decreases. It is suggested that a competitive relationship between embryos with different genotypes is established as early as at the preimplantation stage.