Coat Color Locus Research Articles

The effects of selection and human preference on coat colour gene frequencies in urban cats.

In an attempt to examine the possibility of selection on domestic cats populations in the urban environment, a number of surveys were conducted in four contrasting areas of Glasgow--two near either extreme of Western, industrial socioeconomic status. The first survey was in the form of a questionnaire to inhabitants enquiring of preference for a particular phenotype. This survey revealed a consistent preference for lighter phenotypes in all areas. The incidence of cat ownership was greatest in the two affluent areas where there was also a high risk of the cat being sterilised. Independent of the questionnaire survey was a study of cat coat colour gene frequencies in each of the four districts. This study revealed that darker phenotypes predominate in the two areas of lower socioeconomic status, Maryhill and Govan. To date, the cat populations in these two areas are the darkest to have been described in the world. In contrast, a lighter phenotype was found in cats inhabiting the two districts of higher socioeconomic status, Kelvinside and Bellahouston. This difference in phenotypic darkness was also paralleled by appropriate clines in coat colour gene frequencies. The results demonstrate that human preference is not effectively translated into selection at any of the loci considered. In situations where human preference is most likely to occur, neutering risk is also high. Although the force responsible for the darkening of phenotype has yet to be identified, the fact that the darker alternative allele at each of the O, a, t, d, S and W loci is favoured suggests that selection is operating on these polymorphic coat colour loci.

GENETIC CONTROL OF THE ANTIBODY RESPONSE IN INBRED RATS

SUMMARYThe primary and secondary responses of rats to SRBC, measured by means of haemolytic antibody titres, showed strain differences. High‐responder strains produced high levels of antibodies of IgG and IgM. Low‐responder strain produced only low level of IgM antibody. With subsequent antigen challenge, only the high‐responder strains produced high titres of antibody. Low‐responder strain, in contrast, continued to make a low level of IgM antibody. Allogeneic transfer of spleen cells changed the low‐responder strain, Fischer rats, to produce anti‐SRBC IgG antibody. Fischer rats also showed low responses to OVA, BGG and to some ‘thymus independent antigens’. Genetic analyses showed the antibody production against SRBC and BGG was controlled by a single gene respectively. No linkage was found between Ir‐SRBC, Ir‐BGG, R (major histocompatibility) and c (coat colour) loci.

Gene frequencies in stray cat populations from Vienna

A sampling of 394 cets from Vienna was taken and the gene frequencies for different coat colour loci calculated. Randomness of breeding was tested by the Hardy-Weinberg distribution. A comparison of Viennese data with those of other city populations gives the impression that cat populations of Middle Europe have their own stable gene pool, which differs significantly from North-West Europe, America and Australia.

Defects in hematopoietic differentiation in NZB and NZC mice.

Hematopoietic stem cell activity in inbred NZB and NZC mice has been determined by transplantation and endogenous spleen colony assays. Whereas NZB mice show normal colony-forming unit (CFU) activity in the transplantation assay, they show markedly elevated endogenous CFU. NZC mice also show this markedly elevated endogenous CFU activity, but in the transplantation assay show only about 5-10% of normal CFU counts. When NZC stem cells are tested for CFU activity in irradiated recipients of the H-2(d) type, almost normal colony numbers occur. NZB stem cells however also cannot form colonies in NZC mice. These results suggest that NZC mice have a defect in the micro-environment of the spleen which renders them incapable of allowing transplanted CFU to form colonies. Genetic analysis of both the NZC defect as a CFU recipient, and the elevated endogenous count in NZB and NZC, shows that both are controlled by single recessive genes which are not linked to either coat color, agouti, H-2 or Ig loci. Of even more relevance is the finding that these hematopoietic abnormalities are not linked to the genes involved in controlling autoantibody formation to red cells in the NZB mice. These mice therefore appear to show two distinct hematopoietic abnormalities, the analysis of which may be of considerable value in understanding the detailed events of hematopoietic stem cell differentiation.

Natural mutation rates in the house mouse estimates for five specific loci and dominant mutations

More than 7 million mice were examined for grossly visible spontaneous mutations. A total of 249 mutations were recovered, of which 206 could be characterized as their mode of inheritance (dominant or recessive). The rates of spontaneous mutations at 5 specific coat-color loci ( a, b, c, d, and ln) were 11 · 10 −6 per locus per gamete for mutations from wild-type, and 2.5 · 10 −6 for mutations from recessive alleles. Large differences were found between the rates of the individual loci; the a, a +, and c + alleles had the highest rates. Estimates of “forward” and “reverse” mutations at each of these five loci also showed large differences. A comparison of the rates at the five specific loci and those at other loci for which dominant mutations were recovered showed that the specific loci used in this study had a spontaneous mutation rate 6 times higher. No effect of the age of parent was discernible for those loci where sufficient numbers of mutants were recovered to make a meaningful comparison.

Role of linkage in gene frequency change of coat color alleles in mice.

ASSOCIATION between characters can be ephemeral, as that caused by linkage; or more persistent, as that caused by the pleiotropic effects of one or more genes. In the event of an association due to pleiotropy, selection for one character should produce a correlated response in the other of greater regularity and continuity than if the association was the result of linkage. Mice of both the brown and dilute phenotypes have been observed to be larger in body size than non-mutants (FELDMAN 1935; GREEN 1935; CASTLE et al. 1936; CASTLE 1941). Several studies have attempted to determine whether these observations are the result of genes influencing body size linked to the coat color loci or the pleiotropic effect of the mutants on body size. GREEN ( 1935) compared the body size of brown (bb) and heterozygous black (Bb) mice in various back-crosses involving different homozygous parent lines. He found that the body size difference between color genotypes varied from one backcross to another. In interpreting these observations, he hypothesized that this was caused by linkage between the brown locus and genes affecting body size. CASTLE et al. (1936) made a number of body size measurements on both brown and dilute (dd) mice and their black and non-dilute (D-) sibs in backcross and F, matings. The larger size which they found associated with mice having the recessive phenotypes they attributed to the physiological effect of the brown and dilute alleles. MACARTHUR (1949) reported in a two-way selection experiment for body weight that his high line was mostly bb dd and his low line mostly BB DD. He felt this corroborated CASTLE'S data and demonstrated that the brown and dilute alleles have a pleiotropic effect for larger body size. BUTLER (1954) crossed bb dd mice from MACARTHUR'S high line with two different inbred lines homozygous for the non-dilute (D) allele and compared body size in F, and backcross mice classified according to dilute or non-dilute coat color. He found that non-dilute mice were slightly larger in both the F, and backcross tests. BUTLER also examined an inbred line which was segregating for the dilute locus. After maintaining this line for seventeen generations and selecting only for general vigor, he again found that non-dilute mice were slightly larger than dilute mice. BUTLER noted that his results, while statistically nonsignificant were similar in magnitude to those reported by CASTLE but opposite ' SLientifiL Iournal .biicle No 0318. blmnesota 4gnculture Expninient StatLon lhe woik W~S suppurled bg the ~dtl~Jrld~ Science Foundation, Giants G 8878 and GI3 12%

Linkage of one component of the major urinary protein complex of mice to the brown coat color locus

Two codominant alleles,Mup-a1andMup-a2, controlling electrophoretic variation of one of the components of the major urinary protein (MUP) complex of the mouseMus musculushave been found to be linked to the black–brown coat color alleles (linkage group VIII).

Spontaneous mutation rates at five coat-color loci in mice.

Examination of 1.5 million mice yielded natural mutation rates estimnated from 5.2 million gene reproductions at five specific coat-color loci. The average rates were 11.1 x 10(-6) for forward mutations and 2.7 x 10(-6) for reverse mutations. Differences between the frequencies of mutations at the individual loci were evident.

Natural mutation rates in the house mouse: plan of study and preliminary estimates.

Abstract From the autumn of 1963 to the summer of 1964, 630320 mice in 18 inbred strains and 173754 mice in six F 1 hybrid generations, produced under regular laboratory conditions, were examined for presumptive natural mutations at any one of five specific coat color loci and at any other locus as well. Altogether 40 of 303 presumptive mutations have proved to be mutations. The preliminary estimates of reverse (recessive to dominant) mutation rates are: 6.5·10 −6 for nonagouti ( a ) to alleles a t adn A w ; 3.6·10 −6 for dilution ( d ) to wild type ( d + ); o for the brown ( b ), albino ( c ), and leaden ( ln ) loci. The preliminary estimates of forward (dominant to recessive) mutation rates range up to 30·10 −6 for the ln locus. Other estimates are 1.1·10 −6 for the tabby ( Ta ) locus and 4.9·.10 −6 for the dominant spotting ( W ) locus. The occurrence of gonadal mosaics may eventually be a means of studying the mutability of genes in cells at all stages of development.