To investigate the cellular action of the Miωh allele in the mouse with regard to its effects upon coat color patterns, we generated a series of aggregation chimeras, using embryos that differ in their mi locus genotype. We have obtained 11 chimeras Miωh/ + C/C↔ + / + c/c and 8 chimeras + / + C/C↔ + / + c/c. Chimerism was determined by coat and retinal pigment epithelium mosaicism and by the electrophoretic analysis of GPI-1 isoenzymes. In Miωh/+ C/C↔, +/+ c/c mice white coat color prevailed due to the higher percentage of unpigmented areas and the higher percentage of unpigmented hairs in pigmented areas. Our data indicate that a single Miωh gene dose decreases the melanoblast proliferative activity, causing the lightening of coat pigmentation. In Miωh/ + C/C↔+/+ c/c mice a few pigmented hairs were often detected on the belly where Miωh / + mice always had a white spot. This suggests that in the chimeras the presence of some non-Miωh cells in the skin of the belly allows pigment cells to develop. Using embryos of two substrains of Miωh/Miωh mice that differ in their Gpi-1 locus genotype we have produced 8 Miωh/ + ↔ Miωh/Miωh chimeras. In all these chimeras coat color patterns resembled those of Miωh/ + heterozygotes despite the higher percentage of the Miwh/Miωh component in three chimeras. Mosaic hairs were absent in the chimeras. This shows that the chimeras have only one Miωh/ + melanoblast population which actively proliferates and colonizes almost all hair follicles. Thus the Miωh/Miωh dermis and epidermis do not suppress proliferation and differentiation of the Miωh/ + melanoblasts except the certain area on the belly.

Genetic variation in 40 domestic rabbits (Oryctolagus cuniculus) from eight different strains was investigated by horizontal starch gel electrophoresis. Twenty nine enzyme systems were examined in different tissues, 10 isoenzymes were found to be polymorphic. Indices of genetic variation show values comparable to those found in most other mammalian species. Thus the unusually high values reported previously by other authors may be due to a limited and not randomly chosen set of enzymes studied.

Wehrhahn (1975) introduced the method of probability generating function to study the distribution of charge differences between homologous proteins in a population but considered only the special case where the population starts with a single allele. Some of his results, however, contained errors. In this paper, all the formulae are presented in general, correct yet much simpler forms. It is also shown that the method of diffusion equations (Ohta & Kimura, 1973) can produce the same results. Numerical computations show that the difference between the one-step and two-step models of charge changes is practically negligible. The results obtained have also been applied to study Nei's genetic distance. Numerical computations indicate that the genetic distance computed from electrophoretic data is about 10% smaller than the expected number of amino acid substitutions involving charge changes in the early stage of divergence of populations and may give a serious underestimate in comparisons between species.

Two inbred strains of mice differing in the mean percentage of spermatozoa with abnormal heads were used: KE (16·1%) and CBA (5·9%). The F1 resulting from the crosses exhibited a heterosis effect, while in the backcrosses an obvious segregation of genotypes was observed; both generations showed a reciprocal difference, depending on the source of the Y chromosome. The character of sperm head abnormality seems to be polygenically determined, one of the genes being located on chromosome Y.

Seven generations of backcrosses were performed in which the Y chromosome from CBA was introduced to the genetical background of the KE strain. In the seventh generation 10·2% of abnormal spermatozoa were found, which is significantly lower than in the KE strain. The difference shows the net effect of the Y-linked locus. A correlated difference was found in the fertilization rate, indicating that a factor influencing male fertility is located on chromosome Y. It does not seem to influence the shape of normal spermatozoan heads.

Karyotype analysis did not reveal gross abnormalities in the KE strain.

Recombination between the t6 complex, three allozyme-encoding loci, two antigen-encoding loci, and four molecular markers was studied. The allozyme-encoding loci were complement component-3 (C-3), kidney catalase (Ce-2), and glyoxalase-1 (Glo-1); the antigen-encoding loci were the H-2 Class I genes H-2K and H-2D; the four molecular markers were Tu66, an α-globin pseudogene (Hba-4ps), an unidentified H-2 Class I gene, and the H-2 Class II gene I-Aβ. The latter six loci were used as markers for the t complex. Recombination was detected between Glo-1, Ce-2 and C-3, but not between the markers for the t complex Tu66, Hba-4ps, and the H-2 loci. These data indicate that Ce-2 and C-3 are located outside the t6 complex, while the latter are located within. These data also indicate that the telomeric boundary of the t6 complex is located between H-2 and Ce-2. Recently published studies have shown that complete gametic disequilibrium exists between the t complex and loci located centromeric to the H-2 - Ce-2 interval, while disequilibrium was not detected between loci located telomeric to this interval. Loci included within the region of recombination suppression are also those in disequilibrium with the t complex. As a result, recombination suppression probably resulting from chromosomal rearrangements associated with the t complex appears to be a sufficient explanation for the gametic disequilibrium observed between certain loci and the t complex.

Cytoplasmic petite mutants, spontaneous and induced, show various patterns of ability υ. inability to utilize the sugars galactose, α-methylglucoside and maltose, depending on the strain from which they were isolated. Petites recombine and segregate their different sugar deficiencies among vegetative diploid progeny when crossed, indicating mitochondrial control. Crosses between petites and wild-type further indicate that mitochondrial factors may be interacting with nuclear factors in a complex regulatory system.

A gene, Hst-3, responsible for sterility in F1 males from crosses between Mus spretus and laboratory strains of mice such as C57BL/6, has been localized on the distal part of the X chromosome, using both DNA probes and biochemical markers on a panel of Fl(C57BL/6 × SEG) × C57BL/6 backcross males. This gene may be a model for studying mammalian hybrid sterility.

Colicin factors Ib-P9 and Ela-16 both convert their hosts to chromosomal donors. However, negative fluctuation tests suggest that chromosomal transfer does not result from the formation of stable Hfr variants.

Thirty-one inbred strains were tested for their reaction to drinking water which contained a low concentration (10−4 M) of sucrose octaacetate (SOA). One strain, SWR, showed a strong aversion to drinking the SOA solution. The other thirty strains, and two samples of wild-derived mice, tended to prefer the SOA solution to untreated drinking water. The pheno-typic difference between SWR and the other strains was shown to be determined by an autosomal gene. The allele present in SWR is dominant. The gene is not closely linked to jerker (je), pearl (pe) or waved-2 (wa-2).

We have isolated a number of λ dg HFT lysates which carry proximal fragments of the galactose operon. Most of these have been shown to be different, and each terminates in either the kinase or transferase cistron. They divide the kinase cistron genetically into seven blocks of mutants, and the transferase into eight.

When a λ dg is used to transduce a bacterium which carries a mutation in a cistron which is intact in the λ dg the transduction frequency is high in the presence of λ-helper. This is attributed to integration of the transducing fragment at the λ-attachment site and complementation between the two operons in the heterogenote. When the same λ dg transduces a mutation lying in the cistron in which the λ dg terminates, so that recombination within the galactose operon is obligatory, the transduction frequency is 10 to 1000 times less.

In such cases there is a general increase in transduction frequency between distal mutations (i.e. those lying near the termination of the deletion) and proximal mutations, but the relationship does not hold for many individual pairs of mutants, probably due to physiological differences between the bacterial strains.

DNA sequencing and restriction mapping provide us with information on DNA sequence evolution within populations, from which the phylogenetic relationships among the sequences can be inferred. Mutations such as base substitutions, deletions, insertions and transposable element insertions can be identified in each sequence. Theoretical study of this type of sequence evolution has been initiated recently. In this paper, population genetical models for sequence evolution under multiple types of mutation are developed. Models of infinite population size with neutral mutation, infinite population size with deleterious mutation and finite population size with neutral mutation are considered.

In a search for genetic differences in susceptibility to cleft lip with or without cleft palate [CL(P)], congenic and recombinant inbred strains of mice were treated with phenytoin or control injections. Of six loci tested, five were found to affect susceptibility to phenytoin-induced and/or sporadic CL(P): (1) the major histocompatibility locus, H-2; (2) the locus controlling β2-microglobulin, B2m; (3) a locus controlling β-glucuronidase, Gus; (4) the locus controlling N-acetyl transferase, Nat; and (5) the locus for brown pigmentation, b. B2m and Gus only affected the sporadic incidence of CL(P), while the b locus only affected phenytoin-induced incidence of CL(P). Three of these loci are also known to affect glucocorticoid-induced isolated cleft palate (CP), but different alleles of the loci are involved. Phenytoin did not affect levels of adenosine 3′,5′-cyclic monophosphate (cAMP) in palates and tongues of day 15 fetuses. A comparison of glucocorticoid receptor parameters with the incidence of phenytoin-induced CL(P) found no correlation.

Classical population genetic models show that disruptive selection in a spatially variable environment can maintain genetic variation. We present quantitative genetic models for the effects of disruptive selection between environments on the genetic covariance structure of a polygenic trait. Our models suggest that disruptive selection usually does not alter the equilibrium genetic variance, although transient changes are predicted. We view a quantitative character as a set of character states, each expressed in one environment. The genetic correlation between character states expressed in different environments strongly affects the evolution of the genetic variability. (1) If the genetic correlation between character states is not ± 1, then the mean phenotype expressed in each environment will eventually attain the optimum value for that environment; this is the evolution of phenotypic plasticity (Via & Lande, 1985). At the joint phenotypic optimum, there is no disruptive selection between environments and thus no increase in the equilibrium genetic variability over that maintained by a balance between mutation and stabilizing selection within each environment. (2) If, however, the genetic correlation between character states is ± 1, the mean phenotype will not evolve to the joint phenotypic optimum and a persistent force of disruptive selection between environments will increase the equilibrium genetic variance. (3) Numerical analyses of the dynamic equations indicate that the mean phenotype can usually be perturbed several phenotypic standard deviations from the optimum without producing transient changes of more than a few per cent in the genetic variances or correlations. It may thus be reasonable to assume a roughly constant covariance structure during phenotypic evolution unless genetic correlations among character states are extremely high or populations are frequently perturbed. (4) Transient changes in the genetic correlations between character states resulting from disruptive selection act to constrain the evolution of the mean phenotype rather than to facilitate it.

Introducing a new genetic model called the discrete allelic-state model, the evolutionary change of genetic variation of quantitative characters within and between populations is studied under the assumption of no selection. This model allows us to study the effects of mutation and random genetic drift in detail. It is shown that when the allelic effects on phenotype are additive, the rate of approach of the genetic variance within populations to the equilibrium value depends only on the effective population size. It is also shown that the distribution of genotypic value often deviates from normality particularly when the effective population size and the number of loci concerned are small. On the other hand, the interpopulational variance increases linearly with time, if the intrapopu-lational variance remains constant. Therefore, the ratio of interpopulational variance to intrapopulational variance can be used for testing the hypothesis of neutral evolution of quantitative characters.