NMRI/Han mice ovulate significant numbers of diploid oocytes after gonadotrophin stimulation, most of them arrested at metaphase I. In contrast, females from other mouse strains ovulate only oocytes having completed meiosis I. We investigated the heritability of the trait Dipl I by analysing F1 hybrid females from crosses between the sensitive NMRI/Han stock and two mouse strains (C3H/HeHan and BALB/c) considered as non-sensitive, and females from backcrosses to NMRI/Han males (only crosses with C3H/HeHan). The results show (1) that the trait Dipl I is inheritable; (2) that an X-chromosomal (location proximally from the X–Y pairing region) or autosomal recessive mode of inheritance is excluded; and (3) that the expression of the trait, measured as frequency of diploidy, is modulated by a maternally transmitted factor.

Over one hundred backcross-one progeny were analysed by two dimensional electrophoresis to locate the genes on the short arm of chromosome 1D which code for, or control, the D group of LMW glutenin subunits. Recombination between these genes and Glu-D 1, encoding HMW glutenin subunits, was frequent but none could be detected between the D subunit genes and Gli-D1, coding for ω-gliadins, γ-gliadins and the B group of LMW glutenin subunits. These results are in contrast to those for chromosome 1 B because apparently homoeologous D subunit genes occur at a different position, being equidistant between Glu-B 1 (homoeologous to Glu-D 1) and Gli-B 1 (homoeologous to Gli-D 1). A range of 18 genetically-diverse wheat varieties, each containing one of two allelic groups of 1 D-encoded D subunits, were also analysed by two-dimensional electrophoresis. Consistent with the genetic analysis above, unbreakable linkages were found between these alleles and alleles of Gli-D 1. The results are discussed in relation to the evolution of the distribution of prolamin genes in the wheat genome.

The rudimentary locus of Drosophila melanogaster contains the structural information for the first three enzymes of the de novo pyrimidine pathway. Two new rudimentary (r) mutants have been isolated following mutagenesis with ICR-170. From complementation analysis and cyto-genetical observation both were shown to be deficiencies which expose the r locus. Df(1)r19 is deleted from band 14D1 to 15D1 and Df(1)r1D from band 14B6 to 15A2. These deficiencies were combined with several characterized r alleles each giving a single enzymatic defect in one of the first three enzymes of the pyrimidine pathway. An unusual semilethal trans effect was observed in some but not all the combinations. The effect was not observed with a third smaller deficiency which also exposes the rudimentary locus.

Internal sequences of Tn501(Hg) and Tn721(Tc) have been compared by hybridization. In spite of the difference in the resistance they code for, there is extensive homology between the two elements. This homology resides in the transposon-coded genes that are necessary for transposition and indicates that the elements are closely related.

Aggregation chimaeras were made from embryos of strains of mice selected for large and small body size and of unselected controls. The strains were combined in pairs marked by albino coat colour and by allo-zyme variants at the Gpi-1 locus. The proportion of cells derived from each component was scored visually in the coat melanocytes and by electrophoresis in ten other organs or tissues (blood, liver, lung, spleen, spinal cord, brain, pituitary, kidney, adrenal and testis). The object was to find out how body weight is related to cell proportions in the body as a whole and in the separate organs. Individuals varied widely in their mean cell proportions but there were significant differences between organs within individuals. Body weight was linearly related to the mean cell proportions which accounted for most, or possibly all, of the chimaeric variance of body weight. No one of the organs studied could be identified as being solely responsible for growth control, or as having a predominant influence on growth. The weights of some organs were probably influenced to a small extent by their own cell proportions independently of the individual's mean, but the differences of body weight were too great to be accounted for by the summation of localized effects on organs. The mean cell proportion, averaged over individuals, was close to 50%, proving that there was no tendency for cells from the larger component to outgrow those from the smaller. It is concluded that growth control must be systemic, but it was not possible to decide whether the systemic effect comes from some particular organ not studied, or is in some undefined way the consequence of the cell proportions in the body as a whole. There was some evidence, though it was inconclusive, that chimaeras show ‘heterosis’ for body weight.

Using mice that were mosaics for both Xce and phosphoglycerate kinase (Pgk-1) alleles, we present further evidence that the parental source of the X chromosome may affect the probability of that X chromosome remaining active. The reciprocal cross differences in PGK-1 activity described here are intermediate between those published previously for other alleles of Xce.

When the mutant veinlet was removed from a Drosophila melanogaster line selected for shortened vein length it was found that the selected polygenic background produced vein gaps in the absence of the major mutant. This example of genetic assimilation was unusual, however, in that the phenotype of the assimilated line was not exactly the same as the phenotype of the original selection line. It differed in two respects: only one of the longitudinal veins was affected in the assimilation line whereas all veins are shortened in the selected ve line, and vein gaps were sub-terminal in the assimilated line whereas they are terminal in veinlet. Modifiers of L 4 vein length were found to be located on both chromosomes II and III, though the chromosome II factor had a larger effect and was required for gap formation. The chromosome II gene was mapped to the same position as a similar L 4 vein length polygene (PL(2)L4a) found in another veinlet selection line and reported elsewhere. The pattern of expression of the ve mutant and the assimilated line genotype were compared using profiles of vein frequency at given points. The vein pattern profiles are discussed in relation to an hypothesis to explain the observed selection response and the effectiveness which these polygene combinations showed in modifying the much more complex veinlet phenotype.

Patterns of P element establishment and evolution were compared in populations of D. melanogaster and D. simulans. For each species, mixed populations were initiated with M strain flies lacking P elements together with P strain flies having similar P element copy numbers and phenotypes. The mixed populations were subsequently maintained under similar environmental conditions. On the basis of gonadal sterility assays, P elements tended to be significantly more active in D. melanogaster than in D. simulans populations. This activity difference between the two species was positively associated with P element copy number, determined by restriction enzyme analysis, and transposition frequency, as determined by a transposition assay. Host factors are the most likely explanation for the observed species variation. Difficulty of establishment may be a factor determining the absence of P elements in natural populations of D. simulans.

Six axonemal mutants of Paramecium tetraurelia have been isolated that are unable to respond properly to calcium. The mutants, designated atalantas, cannot swim backward when stimulated by ions or heat. Genetic analyses reveal that all six mutants are recessive and fall into four complementation groups. Three of the mutants in one complementation group are phenotypically non-leaky, one is leaky and two are extremely leaky, only displaying their phenotypes at elevated temperatures. The complete mutants, ataA, are also abnormal in their forward swimming. This abnormality co-segregates with the inability to swim backward. ataA1 is not allelic to several membrane mutants of P. tetraurelia.

The effect of selection on individual performance for a quantitative trait is studied theoretically for populations of finite size. The trait is assumed to be affected by environmental error and by segregation at a single locus. Exact formulae are derived to predict the change in gene frequency at this locus, initially by finding the probability distribution of the numbers of each genotype selected from a finite population of specified genotypic composition. Assuming that there is random mating and no natural selection the results are extended to describe repeated cycles of artificial selection for a monecious population. The formulae are evaluated numerically for the case of normally distributed environmental errors.

Using numerical examples comparisons are made between the exact values for the predicted change in gene frequency with values obtained using approximate, but simpler, methods. Unless the gene has a large effect (α) on the quantitative trait, relative to the standard deviation of the environmental errors, the agreement between exact and approximate methods is satisfactory for most predictive purposes. The chance of fixation after repeated generations of selection is also evaluated using the exact method, and by means of a diffusion approximation and simple transition probability matrix methods. Except for very small values of population size (N) and large α the results from the diffusion equation agree closely with those from the exact method. Similar results are found from tests made of the prediction from the diffusion equation that the limit is only a function of Nα for a given intensity of selection and initial frequency, and that the rate of advance in gene frequency is proportional to 1/N for the same set of parameters.

We have studied, using light microscopy, the relationship between chromosome content and nuclear diameter in early spermatids of males carrying different combinations of wild-type and compound chromosomes in Drosophila melanogaster. By using these genotypes we have been able to observe spermatid nuclei bearing various numbers of chromosomes ranging from only one sex chromosome and no major autosomes to almost twice the normal chromosome complement. We have found that variations in the chromosome content are accompanied by increasing the variance in early spermatid nuclear diameter; the more gametic classes produced, the higher the variance of nuclear diameters. These results indicate that measuring nuclear diameters in early spermatids represents a useful way to estimate the levels of meiotic non-disjunction and thereby to improve the characterization of lethal or male sterile mutants in which analysis of meiotic chrosome non-disjunction cannot be achieved by conventional genetic methods.

Twenty-nine strains of mice were tested for their ability to taste a 0·8 mM solution of quinine sulphate. There were large strain differences, some strains (tasters) showing a strong aversion to the quinine and other strains (non-tasters) showing very little aversion. It was shown that the difference between strains 129/Sv and A2G is probably due to one gene. By using the CXB RI strains it was also shown that the difference between C57BL/6By and BALB/cBy is probably due to one gene. It is suggested that both differences may be due to the same gene, named Qui. In the progeny of a backcross involving both Soa and Qui there was evidence of an interaction between the genes which cannot be explained satisfactorily. Learning behaviour by the mice influenced their drinking habits, but this did not invalidate the results.

The effects of partial inbreeding on effective population size and rates of fixation of mutant genes are investigated in selected populations. Truncation selection and an infinitesimal model of gene effects for the selected trait are assumed. Predictions of effective size under this model are given for partial selfing and partial full-sib mating and an extension to a more general model is outlined. The joint effect of selection and partial inbreeding causes a large reduction in the effective size relative to the case of random mating. This effect is especially remarkable for small amounts of selected genetic variation. For example, for initial heritability 0·1 and proportion selected 1/6, the ratio of effective size to population size is 0·10 in populations with about 90% selfing while it is 0·85 in random mating populations. The consequence is a reduction in the fixation probability of favourable genes and, therefore, a reduction in the final response to selection. Stochastic simulations are used to investigate the effects of partial inbreeding and selection on fixation and extinction rates of genes of large effect and of recessive lethals with effects on the selected trait. For genes of very large effect, the effective size is not a critical factor and it is expected that partial inbreeding will be efficient in increasing fixation rates of recessive mutants. Lethal recessives are eliminated more frequently and their equilibrium frequency is lower under partial inbreeding, but only when their effects on the heterozygote are not very large.

For a population undergoing mass selection, derived from an unselected base population in generation zero, the expected long-term contribution to the population of an ancestor from generation 1 was shown to be equal to that expected during random selection multiplied by (where is one half the breeding value of the ancestor for the trait under selection standardized by the phenotypic standard deviation, i the intensity of selection, and is the competitiveness which is defined by the heritability in generation 2 and k the variance reduction coefficient). It was shown that the rate of inbreeding (ΔF) could be partitioned into three components arising from expected contributions, sampling errors and sampling covariances respectively. Using this result ΔF was derived and shown to be dominated by terms that describe ΔF by variance of family size in a single generation plus a term that accounts for the expected proliferation of lines over generations from superior ancestors in generation 1. The basic prediction of ΔF was given by

where M and F are the numbers of breeding males and females, T the number of offspring of each sex, ρm and ρt are correlations among half-sibs in generation 2 for males and females respectively, and K is a function of the intensity and competitiveness.

The melanotic tumour gene tu bw of Drosophila melanogaster has a specific suppressor su-tu. The genotypes tu bw; +su-tu and tu bw; su-tu show opposite responses, as measured by tumour penetrance, to increasing choline levels in the defined axenic medium. The three major metabolic functions of choline have been examined using additions to the axenic medium to determine which biochemical pathway(s) are different in the two genotypes. It is concluded that the opposite strain responses are due to changes in the pattern of phospholipid synthesis, and that the gene product of the su-tu gene probably functions in this area of metabolism.