When an R determinant for streptomycin is transferred into a conditionally streptomycin-dependent E. coli B mutant—which requires in minimal medium either histidine or streptomycin—the latter behaves like a histidineless strain. This phenotype modification shows that the repairing action of streptomycin is prevented. The specific requirement of the strain is not now replaced even by streptomycin concentrations up to 10000 µg/ml at which the conditionally streptomycin-dependent mutant could originally grow, and which are well beyond the resistance level characteristic of the R determinant itself. These data seem to suggest that a reduction in permeability of the cell membrane cannot be held responsible for the phenomenon observed.

Within the genus Apodemus, DNA from A. sylvaticus and A. flavicollis could be distinguished on the basis of reciprocal DNA/DNA annealing in agar, even when unfractionated DNA was used. In preliminary experiments, DNA from geographical races of A. sylvaticus could not be distinguished, nor could DNA from two closely related species of Peromyscus.

Within the species Mus musvulus, the fast-renaturing fraction of L-cell DNA, separated on a hydroxyapatite column, was able to discriminate between L-cell (originating from the C3H inbred strain) and NZB (New Zealand Black) inbred strain DNA in agar.

A study was made of reproductive performance and embryonic mortality in XO and XX females. In the stock used, the mean litter size of XO females (4·46) was greatly below that of XX ones (8·17). One series of pregnant females of both karyotypes was dissected after 15 days' gestation, and another series after 3½days' gestation. In the former, there was a significantly greater amount of embryonic mortality in XO females both before implantation and at the small and large mole stages. By far the greater amount occurred before implantation. The data from dissections after 3½ days' gestation concerned pre-implantation embryos, since normal embryos at this point are at the late morula or early blastocyst stage. The embryos from XO females contained a large group of obviously and characteristically abnormal ones; they comprised 60/280 of the embryos from XO females, compared with 4/189 of the XX ones. They appeared to have developed abnormally from a very early stage, probably the two-cell stage, and were considered to represent the missing OY class of zygotes. In addition, it was concluded that there was probably an abnormally low segregation of nullo-X gametes from XO females.

FP transfer to recombinant and non-recombinant recipients of Pseudomonas aeruginosa strain I has been investigated under controlled conditions. When transferred to recombinants, the sex factor appeared to enter first and did not seem to be linked to the early chromosome markers. Five to twenty percent of the recipient population were found to be FP+, depending on the time allowed for pairing. Only 40% of the recombinants were FP+ at 90 min. A possible relationship between FP and chromosome has been discussed.

The first mutation step towards ampicillin resistance in Escherichia coli occurs in the ampA gene, and gives resistance to a D, L-ampicillin concentration of 10 μg/ml. Using interrupted conjugation and transduction experiments ampA was found to be located at 82 min on the time scale of Taylor & Thoman (1964). A number of adjacent markers were studied and the probable gene order of the ampA region was found to be argH-metA-uvrA-ampA-purA-fdp-pyrB. Two independent alleles of ampA were cotransduced with fdp+ and purA+. The phenotypic expression of ampA in a purA strain has been investigated.

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.

The first two steps towards increasing ampicillin resistance in Escherichia coli concern the genes ampA and ampB which are located at least 20 min from each other (Eriksson-Grennberg et al. 1965 and the two preceding papers). This paper describes a third class of ampA-containing mutants (designated ampAB) which are resistant to D, L-ampicillin concentrations of 100 μg/ml. When such as F-strain (D31) was crossed to different Hfr strains analysis of the trp+ and proB+ recombinants indicated that resistance genes were located between trp and proB. Altogether five classes of recombinants were produced but only the two genes ampA and ampB were recovered. One interpretation suggested is that the resistance of D31 is due to the presence of ampA and ampB and a chromosomal aberration by which ampA was moved to a position near ampB. It was possible to transduce both intermediate levels of resistance as well as the full resistance of an ampAB donor strain, but the strains produced were unstable. In crosses the presence of ampAB in the recipient reduced the number of recombinants by reducing the number of stable pairs. In an Hfr strain ampAB was shown to give rise to additional difficulties in establishing the cell contact during mating. Some ampicillin resistant mutants also showed decreased ability to propagate the RNA phage MS2.

UV induces lesions in DNA which lead to the death of cells, mutation and, in yeast, intragenic and intergenic mitotic recombination. We have investigated the interaction of two post-treatments, dark holding and photoreactivation, on the frequencies of these events. It was found that dark holding reduces cell death and intergenic recombinants, but causes an increase in intragenic recombination frequency. Photoreactivation reduces cell death and intragenic recombination, but has no effect on intergenic recombination. After dark holding, photoreactivation has no further effect on cell survival or intergenic recombination, but may reduce the frequency of intragenic recombinants. After photoreactivation, dark holding still causes an increase in cell survival and the frequency of intragenic recombination, and reduces the frequency of intergenic recombination.

1. Triticum aestivum ssp. vulgare variety Chinese Spring (2n = 6x = 42) is susceptible to yellow rust caused by Puccinia striiformis while the wild annual grass Aegilops comosa (2n = 14) is resistant to all the physiologic races for which it has been tested.

2. By a backcrossing programme initiated from Chinese Spring × Ae. comosa hybrids, using Chinese Spring as the recurrent parent, a line was isolated with a single chromosome of Ae. comosa, determining rust resistance, added to the full complement of Chinese Spring.

3. The alien chromosome substituted with good genetic compensation only for the chromosomes of homoeologous group 2 of Chinese Spring. This demonstrated that the chromosome determining rust resistance is in homoeologous group 2. It was designated 2M since Ae. comosa has the M genome.

4. In order to induce recombination between 2M and its wheat homoeologues, hybrids were made using Ae. speltoides which has the capacity to suppress the activity of chromosome 5B that normally prevents homoeologous synapsis. A backcrossing programme, using Chinese Spring as the recurrent parent, was reinitiated from the 29-chromosome hybrids carrying chromosome 2M and the haploid complements of Chinese Spring and Ae. speltoides.

5. Selection was practised for rust resistance and ultimately a resistant plant with 42 chromosomes, that formed 21 bivalents at meiosis, was isolated. This plant was heterozygous for a dominant rust resistance allele (Yr8) derived from Ae. comosa. Homozygotes were isolated in its progeny and in this way the rust resistant breeder's variety, Compair, was established.

6. Compair differs from Chinese Spring in its yellow rust resistance which was shown to be determined by a chromosome corresponding to 2D of Chinese Spring. This chromosome of Compair has the short arm, the centromere and a proximal segment of the long arm of chromosome 2M and a distal segment of the right arm of chromosome 2D. The modified chromosome, which is designated 2M/D, arose by homoeologous recombination in the Ae. speltoides hybrid or in the immediately succeeding backcross generations. Chromosome 2M/D carries the Yr8 gene in the proximal segment of the long arm derived from chromosome 2M.

7. In hybrids between Compair and standard wheat varieties, chromosome 2M/D pairs regularly with chromosome 2D so that regular segregation of Yr8 can be expected and Compair treated like any other parental variety in wheat hybridization programmes.

8. This work illustrates the way that homoeologous recombination can be induced and exploited both in cytogenetic analysis in wheat and in practical breeding work. The nature of the meiotic synapsis of chromosome 2M/D with its partial homologues raises questions concerning the means by which chromosome 5B influences the specificity of meiotic synapsis.