When combinations of inhibitors acting on the subunit B of DNA gyrase were tested in Bac. subtilis strains, the growth-inhibiting effect of novobiocin was specifically antagonized by subinhibitory concentrations of coumermycin A1. An antagonism in the opposite direction was not observed.

Two alternative models are proposed, where the supercoiling decrease caused by novobiocin is antagonized by coumermycin.

This phenomenon seems to be characteristic of the Bac. subtilis species.

The ability of hybrid dysgenesis P factors to survive and multiply under conditions of strong negative sterility selection was studied in mixed P and M laboratory cultures. Eight populations were initiated with varying proportions of P and M strains. Mixed populations and controls were maintained for seventeen generations at 27 °C, a temperature sufficiently high to induce maximum frequencies of sterility in dysgenic hybrids. The two components of dysgenesis, P factor activity and cytotype, were monitored every generation for the first ten generations and intermittently thereafter. With one exception, all the mixed populations evolved to the P type indicating that P factors can survive and multiply, despite low initial frequency and strong negative selection against dysgenic hybrids. However, the average level of P factor activity attained at equilibrium was considerably lower than that of the P strain control population maintained under the same conditions. It was also lower than the equilibrium level of P factor activity attained in a similar experiment carried out at a lower temperature, suggesting that selection favoured P factors with weak rather than strong sterility potential.

Expression of three wing-cell death mutants in Drosophila melanogaster was used to survey cryptic polygenic modifiers of cell death in wild type strains. Females carrying the X-linked mutants Beadex-3, notchoid and scalloped were crossed to males from each of 20 isofemale strains. Phenotypic variation in the amount of cell death was measured in F1 mutant males that were heterozygous for polygenic loci segregating in the wild strains. As expected, each mutant uncovered a broad range of polygenic variation among strains. Yet, when cluster analyses were used to evaluate the degree of correlation among the expressions of Bx3, sd and nd, the isofemale strains could be partitioned into a small number of groups that were similar in the effects they had upon the severity of cell death. Chromosome mapping of one cell death suppressor strain demonstrated that different polygenic loci could produce the same phenotype in different mutant backgrounds.

Genetic similarities among 46 strains of rats based on published data involving 93 samples and 28 biochemical loci were assessed using principal coordinate and cluster analysis techniques. Seventeen strains were represented by more than one colony. In ten of these, nominally identical strains differed, and in four cases this was attributed to genetic contamination. A total of 52 genetically different strains were eventually identified. Strains BN and DA were most dissimilar, while strain BP was the most unusual strain over-all. The principal coordinate and cluster analysis showed three main clusters, which could be explained on the basis of linkage disequilibrium for some of the esterase loci in linkage group 5. Among six of these loci only 12 haplotypes were observed, with 24/52 strains having a single haplotype. Re-analysis of loci in linkage equilibrium failed to reveal any important clusters.

All four coat hair types were longer in mice homozygous for angora (go / go) than in wild-type mice ( + / +). This increase in hair length in mutant animals was due to an increase in the duration of the phase of hair growth (anagen VI). When skin recombinants incorporating mutant or wild-type epidermis and dermis were grafted to a nude host, the activity of the mutant was found to be confined to the epidermis.

Mice gaining 3 or more standard deviations above the mean were noted beginning in generation 25 in a line selected for high 21–42 day weight gain. The exceptional growth rate appears to be due to an autosomal recessive gene, based on the following: (1) the exceptional individuals appeared suddenly, in only one of 2 closely related sublines; (2) mating high growth individuals to unrelated, normal size strains produces relatively uniform F1's with mean gains below the mid-parent average; (3) F2's have a distribution markedly skewed towards high gain and a coefficient of variation approximately double that of F1's; (4) true breeding high growth strains can be established in one generation by intermating the largest F2's; (5) intermating normal F2's produces progenies with a distribution similar to the F1 except for a few large segregates; (6) high growth segregates have been obtained in F2's from each of 4 successive backcrosses to the C57BL/6 inbred line. The symbol hg (high growth) is proposed for the postulated gene, which appears to be completely recessive. Frequency of positively identified segregates in F2's and backcrosses is on average less than 25 and 50%, due probably to some overlap of Hg- and hghg distributions. Gain of hghg individuals from 21–42 days is 30–50% higher than of Hg- contemporaries; mature weight is also much higher, while 21-day weight of hghg individuals in segregating litters is slightly lower. Fertility of homozygotes ranges from normal to as much as 40% lower than for comparable Hg- mice; hghg mice are not obese. The gene may provide a useful model for study of regulation of mammalian growth.

Mutation is modelled in two quantitative characters under separate genetic control in a large population. A bivariate pattern of selection acts to correlate the characters and, without pleiotropy, their genetic correlation is due entirely to linkage disequilibrium. Data on spontaneous mutation, the effective number of genes, and the intensity of natural selection on quantitative characters are used to evaluate the models. It is concluded that, even when selection favors a high correlation between the characters, with random mating and no linkage between loci influencing different traits the genetic correlation between characters is likely to be small in magnitude. A genetic correlation of large magnitude can be maintained only if the loci influencing different characters are tightly linked, or there is a high level of inbreeding in the population created by frequent mating between closely related individuals.

From the available electrophoretic data, it is clear that haplodiploid insects have a much lower level of genetic variability than diploid insects, a difference that is only partially explained by the social structure of some haplodiploid species. The data comparing X-linked genes and autosomal genes in the same species is much more sparse and little can be inferred from it. This data is compared with theoretical analyses of X-linked genes and genes in haplodiploids. (The theoretical population genetics of X-linked genes and genes in haplodiploids are identical.) X-linked genes under directional selection will be lost or fixed more quickly than autosomal genes as selection acts more directly on X-linked genes and the effective population size is smaller. However, deleterious disease genes, maintained by mutation pressure, will give higher disease incidences at X-linked loci and hence rare mutants are easier to detect at X-linked loci. Considering the forces which can maintain balanced polymorphisms, there are much stronger restrictions on the fitness parameters at X-linked loci than at autosomal loci if genetic variability is to be maintained, and thus fewer polymorphic loci are to be expected on the X-chromosome and in haplodiploids. However, the mutation-random drift hypothesis also leads to the expectation of lower heterozygosity due to the decrease in effective population size. Thus the theoretical results fit in with the data but it is still subject to argument whether selection or mutation-random drift are maintaining most of the genetic variability at X-linked genes and genes in haplodiploids.

Two substrains of the inbred mouse strain 101, maintained at Harwell and at Neuherberg, and designated 101/H and 101/E1, differed at five of the eight genetic loci tested and it seems very likely that one of these substrains has been genetically contaminated. The available evidence suggests that 101/E1 is probably the contaminated substrain.

Selection theory usually assumes an equally probable contribution of each selected individual to a large ‘gene pool’ from which the individuals to be measured in the next generation are sampled. With unequal contributions it is possible to find several sets of values for N (the number of selected individuals) and fi (probability of contribution of the ith individual) such that the same selection intensity is attained. It is suggested that the set of values producing minimum genetic drift should be chosen in order to increase the long-term response without any reduction in the short-term advance.

The rDNA of five Y chromosome mutants was examined with respect to their insert free (In−) repeat type multiplicity. The In− repeat number of each mutant was correlated with its hemizygous bobbed phenotype and additivity with an X NO bobbed (bb) mutant. Four of these mutants showed a direct relationship between their In− frequency, hemizygous bb phenotype and additivity tests. A fifth mutant, bb1–4, had a sufficient number of In− repeats to ensure viability to the late pupal stage and show additivity; however, the In− repeats genetically behaved as a complete rDNA deletion. Possible mechanisms resulting in the suppression of the bb1–4 In− repeats are discussed.

The details of the paper by Mittwoch et al. (Genetical Research44, 219–224, 1984) listed on the cover should read:

“Mittwoch, Ursula, Mahadevaiah, Shantha and Setterfield, Leslie. Chromosomal anomalies that cause male sterility in the mouse also reduce ovary size page 219”