Data are presented from a balanced backcross experiment involving three linkage group VI markers in the house mouse. These establish the order N–Ca–bt (naked–caracul–belted), and confirm the unusual recombination values reported earlier; the values for male heterozygotes are about 4 times those for the female ones. The linkage group is extended by the linkage of miniature, mn, with N and Ca, here reported. Data are given which establish the order mn–N–Ca–bt; they indicate that the recombination values for males may be greater than those for females for some way to the left of the N–Ca–bt segment.

A cross of a leopard frog heterozygous for the dominant Burnsi gene (B/ +) with a wild-type (+ / +) resulted in a large excess of B/ + progeny. Two descendent lines established by these B/ + progeny are characterized by excess +/ + progeny. These seemingly contradictory data are reconciled by postulating the existence of a dominant subvital gene (Sbv) linked to the + allele of Burnsi in the initial cross. Progeny used to establish subsequent lines were recombinants with Sbv linked to B. This proposed linkage would constitute the first case of linkage between two mutant loci in anuran amphibians.

Among temperature-sensitive mutants of Escherichia coli a strain was discovered requiring D-alanine for growth. It was proved to possess an altered alanine racemase. The structural gene for this enzyme, designated alr, is located between metB and pur A. The properties of the enzyme and its locus suggest that it is not under control of the mechanisms which regulate mucopeptide formation. A suppressor of the alr mutation was discovered near trp, and termed msuA.

The relationship between the transfer systems of several plasmids was investigated, using as criteria complementation of a series of transfer-deficient Flac mutants, the efficiency of plating of F-specific phages, and identification of surface exclusion systems. The transfer systems of ColV2 and ColVBtrp were similar to that of F except for surface exclusion: ColVBtrp specified a surface exclusion system different from that of F, and ColV2 did not specify any detectable system. The transfer system of R1–19 was also similar to that of Flac, but the products of traA, traI and traJ were plasmid-specific. R1–19 determined the same surface exclusion system as ColVBtrp, and this was under the control of the transfer inhibitor. The transfer systems of ColIbdrd and Flac were unrelated. ColEl was transferred by Flac traI− mutants, but not by mutants in other cistrons.

The sex-linked gene, brindled, in the mouse produces a coat-colour variegation in heterozygous females. There is much individual variation in the relative areas of mutant and wild-type colour, but it was not known if any of this variation was genetic. The main object, when the experiments were started, was to test the simple expectation of the Lyon hypothesis, that if X-inactivation is random the variegation should not be modifiable by selection. On the assumption that the variegation is due to X-chromosome inactivation, modification by selection would show that the inactivation process, or some property of the derived cell populations, is under genetic control. Heterozygous females were accordingly selected for the area of coat showing the mutant colour. Selection based on individual phenotypes was ineffective, but four cycles of reciprocal recurrent selection based on progeny-means produced a ‘High’ line with 64% mutant area and a ‘Low’ line with 30% mutant area, from a base population with 53% mutant area. Autosomal modifiers were not responsible for the response; the difference between the selected lines was entirely due to properties of the X chromosomes carrying the brindled gene. The changed properties of the X chromosomes were not restricted to the locus of brindled, but extended at least as far as the locus of tabby. The chromosomes carrying the wild-type allele of brindled were not altered by the selection, but normal X chromosomes from other strains affected the degree of variegation. It was concluded that the difference between the selected lines was due either to non-random inactivation or to somatic cell selection. It was not possible to distinguish between these two mechanisms. The results obtained in these experiments with a structurally normal X chromosome were in all essentials similar to those obtained by Cattanach with his X-autosome translocation.

A strain of Drosophila, homozygous for the variably penetrant gene tu bw, which causes the formation of abnormal masses of melanizing haemocytes (melanotic tumours), has been reared on defined axenic diets containing various sterols, both singly and in pairs. Both optimal and deficient nutritional levels of sterol have been employed, as well as certain sterols inadequate by themselves to support development. The effect of these diets upon probability of tumour formation has been studied in relation to their nutritional adequacy, as defined by the growth-rate, survival, and in one case, adult body-weight.

The results demonstrate a rather complex pattern of interaction between dietary sterols in determining the variables of the phenotype produced, under circumstances suggesting that all the sterols investigated have entered the developing larvae. There is only a partial overall correlation, and occasionally an inverse relationship, between tumour suppressant and growth-promoting properties of particular sterols. Within single molecules, structural sterol features tend to exert their characteristic effects additively upon the phenotype, except for an inadequacy in utilization of molecules containing the Δ7 double bond, which dominates at low concentrations. With pairs of dietary sterols, however, non-additive or ‘saving’ effects are sometimes seen.

It is suggested that the tu bw allele allows the resolution of several discrete developmental functions for sterols and/or their immediate metabolic products in Drosophila, which cannot synthesize its own sterol. However, the molecular nature of these functions is little understood.

The observed dependence of lacuna counts on the growth phase of colicinogenic cultures suggests a relationship between the probability of colicin synthesis, and the number of colicin factors, per cell.