Ethidium bromide and acriflavin-resistant mutants of petite-negative yeast Kluyveromyces lactis were prepared. One kind of nuclear mutation (EBR1) gave resistance to ethidium bromide and correlated sensitivity towards acriflavin. Another nuclear mutation (EBR2) did not affect ‘natural’ resistance of this yeast towards 15 μM acriflavin. Both nuclear mutations mapped at different loci, suggesting lack of linkage. Cytoplasmic mutants resistant to these two drugs were unstable when grown in complete media with dextrose, reverting to a wild-type resistance genotype. When grown in glycerol-containing media these mutants maintained their cytoplasmic drug-resistance conferring factors.

pMO1111, a derivative of FP110 carrying a Tn1 insert, has been used to generate two plasmid primes carrying Pseudomonas aeruginosa chromosome. pMO1112 has been shown to carry the pro-82+ gene and pMO1113 carries argH+ and lys-12+. pMO1112 is considerably more stable than pMO1113 in a recA+ background.

The variability of recombination frequencies between alleles of the ftr cistron is assessed and shown to be normally in the range of ± 25% though occasionally replicates differed by a factor of two and in rare cases even more extremely. It is shown that the variation results from biological differences between separate attempts at the same cross and cannot be ascribed to sampling error or any other controllable cause. In the light of this variability the marker effect alleles already recognized in this cistron are re-examined with a new series of crosses. It is confirmed that marker effect may act to enhance or reduce the recombination frequency but it is shown that enhancement can be expressed in two entirely different ways. There is one type of site which causes a uniform doubling of the recombination frequency in all crosses no matter where the second site is placed in the map. The second type of marker effect enhancement site causes a very great increase in recombination frequency in crosses against relatively closely linked mutants, but its effect diminishes as the distance between the marker effect site and the second site is increased.

The ovalbumin locus and locus II (Lush, 1961) were found to segregate in a closed flock of White Leghorns. Three of the nine expected genotypic classes were absent and from this it is concluded that the two loci are very tightly linked.

The lack of robustness of models of the maintenance of polymorphism in a heterogeneous environment which has been pointed out by Maynard Smith & Hoekstra (1980), applies also to models based on habitat selection, on temporal variation and on density-regulated selection. Only if (partial) dominance ‘switches’ between environments such that the fitness of the heterozygote is always close to the favoured homozygote, is there reasonable robustness. This is true for all models considered. It is argued that there are good reasons for supposing that the favourable allele at a locus may show dominance, although the experimental evidence is still scanty.

Mitochondrial malic enzyme (MOD-2) was found to be missing in partially complementing genotypes between lethal deletion alleles at the albino locus in Chromosome 7 of the mouse. Since such partial complementers survive to adulthood, the absence of normal mitochondrial malic enzyme is compatible with life; however, the sterility of both females and males may be correlated with this enzyme deficiency. Of the six radiation-induced lethal albino mutations, five includedeletions for the Mod-2 locus mapping 1 centimorgan distally from c. Our data indicate that the maximum genetic distance occupied by any of these deletions is 6 centimorgans.

Non-directional asymmetry of paired organs is attributed to developmental ‘noise’. The level of asymmetry is inversely correlated to the degree of developmental stability. Children affected with familial cleft lip ± cleft palate have an increased asymmetry of their dermatoglyphics and molar teeth. The action of polygenes with a quasi-continuous distribution is consistent with this observation.

The inactive-X hypothesis (Lyon, 1961) states that in the normal female mouse only one of the two X chromosomes is genetically active in each cell of the body other than the germ-cells, and that the choice of which X is to be inactivated occurs at an early stage of embryogenesis, and is at random in each cell. The descendants of these cells then abide by the decision so that females are mosaics for two lines of cells and may show a mosaic phenotype if they are heterozygous for a sex-linked gene. One requisite for the validity of this hypothesis is that only one X is necessary for the development of a normal female mouse, and evidence substantiating this supposition is the apparent normality of XO mice (Welshons & Russell, 1959; Cattanach, 1961a, b). On the other hand it has been suggested that XO mice are not fully viable (Russell, Russell & Gower, 1959), but no data on the comparative viability and growth of XO female mice have yet been reported. In the present communication data of this nature, collected in the process of setting up an XO stock, are presented and support the hypothesis that only one X chromosome is necessary for normal female mouse development.

By application of the neutral model of phenotypic evolution, quantitative estimates of the rate of input of genetic variance by polygenic mutation can be extracted from divergence experiments as well as from the response of an inbred base population to selection. The analytical methods are illustrated through a survey of data on a diversity of organisms including Drosophila, Tribolium, mice, and several crop species. The mutational rate of introduction of genetic variance (Vm) scaled by the environmental variance (VE) is shown to vary between populations, species, and characters with a range of approximately 10−4 to 5 × 10−2. Vm/VE for Drosophila viability is somewhat below this range, while hybrid dysgenesis may temporarily inflate Vm/VE beyond 10−1. Potential sources of bias and error in the estimation of Vm are discussed, as are the practical implications of the observed limits to Vm/VE for projecting the long-term response to selection and for testing adaptational hypotheses.

We have previously described strains of Escherichia coli K12 resistant to D, L-ampicillin concentrations of 50 μg/ml (Eriksson-Grennberg et al. 1965; Boman et al. 1967). Such strains were assumed to be double mutants carrying the genes ampA and ampB. We here describe genetic steps which produce strains carrying only the ampB gene. Determinations of resistance showed that ampA increased the resistance provided by ampA+ by a factor of 10–15. AmpB increased the resistance of both ampA and ampA+ by a factor of 2.

R-factors were introduced into two sets of strains with all combinations of ampA, ampB and their wild type alleles. AmpA and the R-factors gave additive effects on resistance, while ampB doubled the ampicillin resistance mediated by ampA as well as by the R-factors. AmpB also enhanced the chloramphenicol resistance of R-factor and of the wild type chromosomal genes. It is suggested that ampB resembles the modifying genes previously described and that R-factors can be useful for the identification of such genes.