A selection experiment for sternopleural bristles in Drosophila melanogaster was undertaken to measure the effect of suppressing crossing-over on chromosomes II and III using the inversions Curly and Moiré marked with a dominant gene, which severely reduce crossing-over. In one set of lines selected wild-type males were mated to selected females, heterozygous for Cy and Mé, and in a parallel set selected males carrying the inversions were mated to selected wild-type females. Because there is no crossing-over in the males in this species, crossing-over is much reduced in the first set and is at its usual level in the second. The effect of the selection was measured on flies which did not carry the inversions. The suppression of crossing-over reduced the advance at the limit by 28 ± 8% for selection upwards and by 22 ± 7% for selection downwards. The segregation ratios of the inversions were observed throughout the experiment. At the end, the proportion of wild-type flies emerging was not different in the two sets of lines. The results are consistent with an assumption of initial linkage equilibrium between loci affecting sternopleural bristles in the base population.

Using four lines derived from a single base population of Lolium perenne by selection for large leaf size (LL), small leaf size (SL), fast rate of leaf appearance (FR), and slow rate of leaf appearance (SR), the inheritance of a number of related characters specifying various aspects of leaf development was studied. F1 and F2 generations were produced for all possible crosses between these four lines.

The genetic differences between the selection lines were largely additive for all characters studied and entirely so for rate of leaf appearance, duration of elongation of a single leaf and for the time interval between the maturation of leaf 3 and the unfolding of the next youngest leaf on the same side of the apex, leaf 5. The non-additive variances noted in rate of total leaf area formation, individual leaf size and its components length and width, and in the rate of leaf elongation, were associated with a tendency towards heterosis in these characters. This was quite marked in some crosses and tended to be larger for the more complex characters, rate of total leaf area formation and leaf size, suggesting that the heterosis was, to a considerable extent, due to interactions between genes controlling component characters.

The data confirmed the earlier finding that the negative correlated selection response between leaf size and rate of leaf appearance was due to a basic association between the maturation of a leaf and the unfolding (onset of rapid elongation) of the next youngest leaf on the same side of the apex. Thus an increase in rate of leaf appearance reduces the duration of elongation of a leaf and this in turn will reduce leaf length. However, the basic association, which seems to be controlled by vascular development of the young leaf, is not entirely invariate.

The frequency of the more common patterns of non-disjunction in Neurospora was studied. Detection of these asci was accomplished by the use of pantothenate requiring strains grown on reduced amounts of pantothenate, so that combinations of dark, pale, and aborted spores provided evidence of non-disjunction. The isolates from five non-disjunction asci were examined in detail and an apparently high frequency of mitotic recombination was detected for presumed disomic isolates. An hypothesis concerning a mechanism of non-disjunction is presented.

The influence of the linkage group II locus y on DDT resistance in Aedes aegypti has been studied in crosses between the Trinidad resistant strain and QS susceptible strain. The y locus influences DDT resistance in both R/R and R/+ larvae. The effect of y may be interpreted as reducing the penetrance of R (RDDT1), which is also located on linkage group II. y+ is partially dominant and incompletely penetrant in its resistance-enhancing role (although in its pleiotropic effect on larval colour it is dominant and fully penetrant). Penetrance of y+ is influenced by an environmental factor, probably associated with the larval diet.

The effect of y on resistance is evaluated in relation to other genetic influences on the expression of RDDT1.

The significance of polymorphism at the y locus is discussed.

Twenty-four reciprocal crosses between two green and six chimera cultivars, containing respectively normal green and mutant white plastids in their germ layers, were analysed for their segregation patterns of green, variegated and white embryos, and for their fertility data.

Analysis of variance of fertility data showed that W × G crosses were generally less fertile than the reciprocal G × W crosses, but this was not correlated with selection against any particular class of embryo.

Analysis of segregation patterns showed that they were essentially the same with a constant female and varying male parent, but change the female and the pattern could be radically altered. The six different mutant females with both constant green males could be arranged in a sequence in which white plastids were increasingly successful, and white and variegated embryos increasingly frequent. A similar sequence was demonstrated with three green females and two constant white males. It was concluded that the major control of plastid inheritance was determined by the female nuclear and plastid genotypes, with the male having only a minor, modifying influence even when male plastids were more successfully transmitted than female ones.

The very low frequencies of variegated embryos in some crosses led to a rejection of the classical hypothesis of sorting-out from mixed cells, and its replacement by the hypothesis that pure green or pure white embryos arise by the replication of only one plastid at a time, whereas variegated embryos arise by replication of both plastids.

We have recently described a chain-forming mutant of Escherichia coli which showed a decreased resistance to ampicillin and several other antibiotics (Normark, Boman & Mattson, 1969). The gene mediating drug sensitivity was denoted envA and by conjugation mapped at 2–4 min. Transduction experiments have now shown that envA is located between leu and azi at 1·5 min. The mapping was facilitated by the finding that envA mediated sensitivity to actinomycin D, rifampicin and gentian violet. The envA locus could be genetically differentiated from the pea locus mediating resistance to phenethyl alcohol (Yura & Wada, 1968). Studies using partial diploids revealed that envA was recessive to its wild-type allele both when located on an episome and on the chromosome.

Assuming that revertants from envA to the wild-type allele could be selected as ampicillin-resistant derivatives, such mutants were isolated and their phenotype characterized. Reversion to ampicillin resistance was accompanied by reversion to insensitivity to actinomycin D. However, not all revertants exhibited wild-type tolerance to rifampicin. Three different ampicillin-resistant revertants were studied genetically. The results indicate that these strains contain suppressor mutations in the envA region of the chromosome. It is suggested that the envA gene, directly or indirectly, affects the EDTA sensitive ‘permeability barrier’ of the surface layer of Escherichia coli.

Strains of Aspergillus nidulans with, a duplicate chromosome segment are mitotically unstable; in addition to phenotypically improved variants, arising following deletions in either duplicate segment, they give morphologically deteriorated types, some with, enhanced stability. In one isolate, deterioration and increased instability were determined by mutation in a duplicate segment; a more stable derivative no longer had this mutation but had one in another linkage group. Another variant, too unstable for analysis, gave derivatives whose single, new mutations were in different linkage groups. It is proposed that deterioration and increased instability result from tandem duplications on either duplicate segment; transposition of these to non-duplicated regions reduces instability. Another 17 variants had a single new mutation each; mutations, possibly clustered, occurred in all linkage groups. In these strains perhaps transposition preceded analysis. Deteriorated variants gave lineages of types with morphological changes caused by further, superimposed mutations. This continued instability is explained as interaction, in fidelity of replication, of non-homologous chromosome segments.

Instability in A. nidulans stems from chromosome imbalance. As imbalance is known or suspected in other cases of instability it may be possible to show common mechanisms for apparently diverse phenomena.

A comparison was made of the amount of penicillinase produced by strains of Staphylococcus aureus carrying chromosomal penicillinase genes, plasmid penicillinase genes and strains carrying both chromosomal and plasmid genes. Plasmid genes were found to produce at least twice as much enzyme as homologous chromosomal genes. The results suggest that there are, on average, two plasmids per chromosome in exponentially growing cells.

Two inducers were used in these experiments—methicillin and 2-(2′-carboxyphenyl)-benzoyl-6-aminopenicillanicacid (CBAP). The latter proved a more efficient inducer than methicillin and this difference was most apparent when more than one i+ gene was present, which suggests that the efficiency of induction reflects the ability of the inducer to react with represser.

Mutants of Hfr strains of Escherichia coli K12 defective in conjugation owing to failure to produce sex pili were isolated by resistance to F-specific phage. Tests of the ability of six de-repressed F-like R factors and four de-repressed I-like R factors to restore Hfr donor behaviour to these mutants indicated that there were several ways in which such restoration could occur. Of a total of 26 defective mutants, 12 were restored by F-like R factors. In these twelve, the function of the integrated F factor was evidently restored, because the sex pili contained F pilin subunits, distinguishable from the R pilin by serological tests. In contrast, among the four I-like R factors, only two were effective, butin all 26 defective mutants; the restored Hfr bacteria produced only I-like pili. The I-like sex factors, in restoring Hfr donor behaviour, did not therefore act by complementing the defective F.

The interrelationship between an F prime and an F-like or I-like R factor was studied in Escherichia coli K 12 strains carrying both. The donorability of such strains suggested that these plasmids were transferred independently by their own transfer systems. Plaque formation by several male- and female-specific phage was tested; the inhibition by Flac of several female-specific phage was not affected by an F-like R factor. Neither did an R factor affect the incompatibility between Flac and Fhis. However, the surface exclusion characteristic of Flac was lost in the presence of an F-like R factor. This is probably closely related to the simultaneous loss of donorability, the F-pilus, and the f+ antigen: all may be the result of the inhibition by an R product of the formation or activity of a single F product.