It is shown that the distribution of the sum of heterozygotes, due to mutant gene(s), that appear in a finite population is invariant under geographical structure, provided that the mutant gene has additive effect on fitness and migration does not change the genetic constitution as a whole population. The expected number of heterozygotes is 2N when Ns = 0 and gradually rises to 4N as Ns increases provided s remains small, where N = the total population size and s = selective advantage of a mutant gene. The distribution of the heterozygosity summed over those generations in which the gene frequency in the entire population is specified, is also shown to be invariant. In the case of a neutral mutant, the density is equal to 4(1 − Y) where Y is the frequency of the mutant in the whole population, and in the selectively advantageous case, it is approximately equal to a constant function 4, provided that the population size times selection coefficient is sufficiently large. These quantities conditional on the fixation of the mutant are shown to be invariant and some special cases are obtained explicitly.

The inheritance of self-incompatibility proteins was studied in three homozygous self-incompatible genotypes of Brassica oleracea var. capitata and their F1 and F2 progenies. The presence or absence in the stigma of incompatibility proteins was determined by immunodiffusion and independently by disk electrophoresis. Certain proteins (antigens) were present in F1 and F2 plants in exact correlation with segregation of the S alleles as determined by phenotypic expression of incompatibility. An S allele–protein–phenotype relationship was thus verified.

Populations of the slug Arion ater rufus sampled from several localities in England and the Netherlands are polymorphic for different electro-phoretic variants of digestive-gland esterase and salivary-gland tetra-zolium oxidase. Samples of Arion ater ater, which is endemic to the British Isles, were found to be monomorphic for these enzymes. Localized populations of A. a. rufus in Britain could have originated from specimens imported accidentally from continental Europe. There is evidence for gene flow between overlapping populations of the two subspecies. In one of the English populations of A. a. rufus, studied in detail, polymorphism for esterase and tetrazolium oxidase is shown to be balanced. Heterosis may be an important factor contributing to the maintenance of balanced polymorphism for tetrazolium oxidase in this population.

A wild strain of Klebsiella aerogenes (V9A), which contains a plasmid Fklac carrying the genes of the lac operon, gives two mutant cell types, recognized by the appearance of their colonies on MacConkey lactose agar. These are referred to as ML− and ML−/+, wild-type being ML+. ML− cells can grow rapidly on 1% lactose as carbon source but very slowly on 0·2% unless induced by TMG or D-fucose, or by previous growth on galactose, melibiose or raffinose, which enables them to grow rapidly on 0·2% lactose for 2–4 cell generations. Previous growth on 1% lactose does not induce the ability to grow rapidly on 0·2% lactose. It is concluded that ML− cells have a defect in the lactose permease gene which allows slow uptake of lactose when the external concentration is 0·2% and more rapid uptake when the external concentration is increased. In addition, TMG, D-fucose, galactose, melibiose and raffinose induce one or more other galactoside permeases which can accumulate lactose efficiently but are not induced by lactose. ML−/+ cells can grow normally on 0·2% lactose as carbon source, but only after a substantial lag when transferred from glucose, glycerol or sucrose, and after an even longer lag when transferred from melibiose or raffinose. Wild-type cells (ML+) grow normally on 0·2% lactose after a short lag of less than a cell generation time, when transferred from any other carbon source. Cells of each of the three phenotypes (+, −/+ and −) can mutate to give both of the other two phenotypes. Incomplete genetic evidence suggests that the ML− mutation is a result of a reversible change in the Fklac plasmid.

Measurements of chiasma frequency over a range of temperatures from 9 to 35 °C in euploid wheat and lines nullisomic for chromosome 5D showed the absence of chromosome 5D greatly to increase the sensitivity of chiasma frequency to temperature, resulting in complete univalence at the lowest temperatures. Careful examination of meiotic prophase showed the lowering of chiasma frequency to be correlated with failure of zygotene chromosome pairing, justifying the use of the term asynaptic. Observation of the pairing behaviour of an isochromosome in the nullisomic 5D background suggested that the asynapsis was due to a failure in the mechanism of chromosome pairing rather than of the pre-alignment of homologues. The observed effects in the absence of chromosome 5D could be due to the presence of a recessive allele at the locus of chromosome 5A, also known to control stability of chiasma frequency to temperature. In conclusion it is pointed out that in euploid wheat the sensitivity of chiasma frequency to temperatures within the normal meteorological range could influence the cytological stability of the wheat crop.

A genotype of wheat deficient for a pair of chromosomes stabilizing chiasma frequency against extremes of temperature was investigated to determine the position and duration of temperature sensitivity with respect to first metaphase of meiosis. Temperature changes over a critical range, followed by sequential sampling and measurement of chiasma frequency, showed a relatively short temperature-sensitive stage, the position and duration of which were dependent on the final temperature used. Comparison with meiotic timings made independently showed that the temperature-sensitive stage occurred in the premeiotic interphase. Euploid wheat was shown to have a stage in chiasma formation sensitive to high-temperature treatments at a similar time.

Comparison with the work of others showed that the sensitive stage lay between the last premeiotic mitosis and the start of DNA synthesis. This modification of chromosome pairing at a much earlier stage than has been previously demonstrated is further evidence that the processes of chromosome pairing and crossing-over are probably more complex than formerly envisaged.

Current molecular models of genetic recombination invoke steps mediated by deoxyribonucleases. It is likely therefore that some mutants deficient in these enzymes would have defective recombination mechnisms. Mutants of Ustilago maydis deficient in extracellular and intracellular DNase activity have been isolated. Three of the extracellular mutants are recessive and non-complementing, as are four of the intracellular mutants. The loci for extracellular and intracellular DNase deficiency have been named nuc-1 and nuc-2 respectively, and they are linked.

In crosses where each parent was deficient in both extracellular and intracellular DNase activity, meiotic allelic recombination (gene conversion) within the nar locus was abolished, although crossing-over in one tested interval was apparently normal in frequency. In DNase-deficient diploids, no mitotic allelic recombination in the nar locus was observed and the distribution of crossing over was abnormal. Nuclease deficiency did not appear to have any strong effect on radiation sensitivity.

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).

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.