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.

The R-factor RP1, which carried the markers amp neo tet, confers resistance to penicillins by specifying the synthesis of Type IIIa β-lactamase. It was detected initially in a strain of Pseudomonas aeruginosa (Sykes & Richmond, 1970) and fragments spontaneously in Ps. aeruginosa strain Ps 18 to give clones which carry only the amp marker. Such clones are said to carry the element RP 1–1 since they are still capable of specifying the transfer of ampicillin and carbenicillin resistance to appropriate recipients in mating experiments. However, unlike lines carrying RP 1, they contain no detectable extrachromosomal DNA (Ingram et al. 1972), and the likely supposition is that the amp gene in these clones has become integrated into the bacterial chromosome together with the regions necessary to allow such strains to act as amp gene donors in mating experiments. It is probably cells of Ps. aeruginosa in which the amp gene has become integrated together with an RTF region that are responsible for the transfer of chromosomal markers reported by Holloway & Stanisich (1971).

An autosomal translocation in the tsetse fly Glossina austeni was studied genetically, cytogenetically and for its effects on viability. Flies homo-zygous for the structural change could be identified by outcrossing to wild-type and demonstrating semi-sterility in all the progeny.

A cytogenetical analysis of male meioses in samples of pupae which were sibs of the semi-sterile progeny showed them to be structurally heterozygous for the translocation. Matings of the translocation heterozygotes and homozygotes gave the expected progeny ratios, with the exception of a deficit of females classified as translocation homozygotes. This was due to their sterility or inviability. Those female homozygotes which did breed showed a subnormal lifetime pupal production. These deleterious recessive effects were probably due to the translocation itself although the influence of linked loci could not be ruled out. These effects would prevent the mass rearing of this particular translocation for a tesetse control project.

Two other stocks which showed semi-sterility were found to carry autosomal translocations and two which currently showed holandric inheritance have Y-autosome translocations. One stock with holandric inheritance of extreme sterility carries a double translocation involving two autosomes and the Y chromosome.

The melanotic tumour gene tu-C4 in Drosophila melanogaster shows incomplete dominance, together with variable penetrance and expressivity. It is tentatively located in the region of locus 52–53 on the third chromosome. Tumour formation in mutant homozygotes involves a precocious haemocyte transformation leading to the appearance of lamellocytes at the beginning of the third larval instar. These aggregate to form tumour-like masses which subsequently melanize. The process of tumour formation is in broad outline similar to that found in other tumour strains. Melanotic tumour formation is treated as a dichotomous threshold character, assuming an underlying normal distribution of liability relative to a fixed threshold. The expression of the tumour gene can be influenced by the levels of protein, phospholipid, nucleic acid and carbohydrate in the larval food medium, and changes in dominance and penetrance induced by sub-optimal environments deficient in these nutrients are positively correlated. Reinforcement by selection of the dominance relations of tu-C4 was accompanied by correlated changes in penetrance. Conversely, selection for increased penetrance was accompanied by correlated changes in dominance. Dominance and penetrance, it is concluded, are fundamentally related aspects of tumour gene expression. Recruitment of dominance modifiers linked to the tumour gene was excluded by the mating scheme employed, and the observed changes in dominance relations in response to selection were due largely to modifiers located on the second chromosome. Changes in dominance relations produced by selection could be significantly reinforced, or reversed, by environmental factors and consequently show a substantial genotype – environment interaction effect. These facts are relevant to current theories of dominance evolution.

The resistance levels conferred by the T-determinants in four R-factors to Tetracycline and Minocycline in cells of Escherichia coli K 12, before and after induction of maximum resistance by treatment with sub-inhibitory concentrations of the drugs, are measured by simple growth-and-challenge tests. The effect of a plasmid TK which confers tetracycline resistance on its host Klebsiella aerogenes is tested in the same way. The five T-determinants fall into a high-level and a low-level group for resistance, the former giving 3- to 4-fold higher resistance in both induced and uninduced cells than the latter. The T-determinants all confer much lower resistance to Minocycline (a tetracycline molecule modified at the C-6 and C-7 positions) than to Tetracycline. The main cause of this difference is that cells carrying a T-determinant exclude Minocycline much less efficiently than Tetracycline, but in addition Minocycline is less effective than Tetracycline in inducing increased resistance. These results are discussed in the light of a model put forward to explain the inducible nature of R-factor resistance to the tetracyclines.

It is argued that the primary break-points for meiotic recombination arise from the replication of regions in which DNA synthesis is delayed until meiotic prophase. The gaps would be in nucleotide chains of opposite polarity in sister chromatids. This would place a restriction on the recombination models of Holliday and of Whitehouse, so that neither is able to explain observed chromatid interference. It follows that if the primary breaks originate in the manner proposed here, the Whitehouse and Holliday models are either both wrong or both right.

Segregation of the prophage of bacteriophage 90 has been observed in reciprocal crosses between lysogenic and non-lysogenic parents of Pseudomonas aeruginosa strain PAO. Linkage of the prophage was shown to three genes determining histidine biosynthesis in that region of the chromosome 7–13 min from the site on the chromosome at which the sex factor FP2 promotes chromosome mobilization.