Spermatozoa from sterile t6/tw32 and control fertile + / +, T/tw32, T/t6 mice were compared for their abilities to hydrolyse protein matrices and for their levels of acrosin activity. The data show that the immature and mature gametes from both the experimental and control males hydrolyse protein matrices. The quantitative acrosin assays show, however, that the mature gametes from the intercomplement males have significantly less total acrosin activity than any of the control groups of gametes. These findings suggest that this reduced acrosin activity is an additional phenotypic expression of the intercomplement genotype which results in male sterility.

Polygenic variation can be maintained by a balance between mutation and stabilizing selection. When the alleles responsible for variation are rare, many classes of equilibria may be stable. The rate at which drift causes shifts between equilibria is investigated by integrating the gene frequency distribution W̅2NΠ(pq)4Nμ−1. This integral can be found exactly, by numerical integration, or can be approximated by assuming that the full distribution of allele frequencies is approximately Gaussian. These methods are checked against simulations. Over a wide range of population sizes, drift will keep the population near an equilibrium which minimizes the genetic variance and the deviation from the selective optimum. Shifts between equilibria in this class occur at an appreciable rate if the product of population size and selection on each locus is small (Nsα2 < 10). The Gaussian approximation is accurate even when the underlying distribution is strongly skewed. Reproductive isolation evolves as populations shift to new combinations of alleles: however, this process is slow, approaching the neutral rate (≈ μ) in small populations.

Parental imprinting effects for chromosome 16 were investigated using disomic animals which were obtained by mating (Rb32Lub × Rb2H) F1 mice. Two allelic forms of the enzyme CuZn-superoxide dismutase, Sod-1a and Sod-1c, were` used to identify maternally or paternally disomic animals. Both types of disomic animals were found with the expected frequencies and did not visibly differ from one another or from non-disomic animals. These results indicate that the genomic imprinting mechanism either does not act on chromosome 16, or, if it does, does not do so in a manner which affects normal development.

Amongst the four common Ha-ras alleles in both controls and cancer patients, we detected the presence of a polymorphic Xho I site associated specifically with the 6·6 and 7·7 kb Bam HI fragments but absent from the 7·1 and 8·2 kb alleles, as recently reported by others. We have extended this study and report here, the consistent appearance of this Xho I site in unusual alleles close in size to the two common alleles of 6·6 and 7·7 kb, in control lymphoblastoid DNA samples in a variety of tumor DNAs. Unusual alleles grouped around the 7·1 and 8·2 kb common alleles on the other hand, did not possess the Xho I site. The consistent presence of the Xho I site polymorphism, in the unusual Ha-ras alleles surrounding the 6·6 and 7·7 kb common alleles and its absence in alleles around the 7·1 and 8·2 kb common alleles, suggests that the unusual ones are derived from the corresponding common alleles to which they are closest in size.

Estimates of the activities (Vmax) of four enzymes that generate the coenzyme NADPH, an absolute requirement for tissue fatty-acid synthesis, and of the concentration of NADP plus NADPH were made in lines of mice differing in fat content. These lines had been selected from the same base population for 20 generations, and 3 high, 3 low replicates and 1 unselected control were used. Analyses were performed on liver and gonadal fat pad (GFP) of males at 5 and 10 weeks of age. In both the liver and the GFP, measurable activities of the four enzymes: glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), isocitrate dehydrogenase (IDH) and malic enzyme (ME) expressed per mg soluble protein were, with minor exceptions, higher in the Fat (F) than in the Lean (L) lines at both ages; the highest ratio being 2–2 for ME in the GFP. The relationships between these measurable activities (Vmax) and in vivo lipogenesis are not however known. When expressed per gram tissue, the ratios for F to L in the GFP were less than 1 in most cases, presumably because of the very different adipocyte numbers and/or sizes between the lines. There were no significant differences between the lines in the concentration of NADP plus NADPH per gram tissue in liver or GFP, suggesting that F lines converted NADP to NADPH faster than L lines. It is predicted that selection on the enzyme activities would be less efficient than direct selection at changing fat content.

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.