Caedobacter taeniospiralis (kappa), a bacterial endosymbiont isolated from Paramecium tetraurelia stock 51, contains, in addition to the bacterial chromosome, covalently closed circular DNA molecules as shown by isolation on dye-buoyant-density gradients. The closed circular molecule has a contour length of 13·75 ± 0·04 µm with a buoyant density of 1·698 g/cm3. The buoyant density of the bacterial chromosome is 1·700–1·701 g/cm3. Kappa of the 51 group isolated from stock 298 and stock 6g2, P. tetraurelia, also contain the closed circular DNA. Two forms of kappa coexist in paramecia: brights and nonbrights. Examination by density-gradient centrifugation of the DNA of brights and nonbrights shows the extrachromosomal DNA to be associated mainly with brights. It is suggested that the extrachromosomal DNA might be the determinant for the refractile bodies and the helical phage-like structures found in brights.

A natural population of the tetrapolar fungus Coriolus versicolor (L. ex Fr.) Quel, in a small woodland was observed over 3 years. Dikaryotic members of the population were identified using intraspecific antagonism and mating type markers. Records were kept of the distribution, longevity and fruiting behaviour of 44 individuals. Zone lines between individuals were found to remain constant in position throughout the study, but rates of decay and fruiting times varied between dikaryons and did not seem related to resource size. Detailed maps of the genetic structure of the populations in two stumps are presented. In general the results indicated thousands of alleles at both mating type loci. Repeated occurrences of alleles were very rare, when the data were interpreted rigorously in terms of the probable origins of the nuclei found in individuals. This approach was also applied critically to some published data. Comparisons were made between alleles found in local and more widely gathered samples, and led to estimation of worldwide frequencies but it is concluded that such exercises are of limited value.

In the mouse histidinaemia has a teratogenic effect. Animals subjected to high levels of histidine in utero may develop inner ear and behavioural abnormalities typical of the ‘shaker–waltzer’ syndrome. Selection procedures for abnormalities and relaxation of selection have resulted in two histidinaemic strains: the Cambridge strain in which abnormalities occur in over 80% of animals, and the Edinburgh strain in which the penetrance of abnormal behaviour has declined to about 1%. Breeding experiments suggest that the differences are largely due to differences in the genetic backgrounds which modify foetal susceptibilities to the teratogenic effects of high histidine levels. High susceptibility appears to be dominant over low susceptibility in the present strains. There appears to be no interaction of maternal histidinaemia with the dreher mutation which is considered to induce inner ear malformation as a result of an early neural tube abnormality.

Seven temperature-sensitive paralytic mutants were recovered from 4544 lines of ethylmethanesulphonate (EMS) treated autosomes in Drosophila melanogaster. These mutants have been designated temperature-induced paralytic (tip). The tip mutations belong to six different genes; four of these, tip-A, Tip-B, tip-C and tip-D are on the second chromosome while tip-E and tip-F are on the third chromosome. This paper describes the paralysing behaviour and genetic localization of the tip mutants.

When a determinant for neomycin-kanamycin resistance (K) was transferred by an F-lac factor into Salmonella typhimurium, the resulting KF-lac strain was sensitive to the male-specific phage μ2 and F-lac was derepressed. However, F-lac alone is repressed in S. typhimurium. When kanamycin resistance is spontaneously lost from S. typhimurium KF-lac an element persists which derepresses F-lac in S. typhimurium. The results are consistent with the hypothesis that a locus der, for derepression of F-lac in S. typhimurium, lies on the K plasmid. The R factor Rldrd19 is derepressed in K12 but is repressed in S. typhimurium. It also is derepressed by der. In contrast to F-lac and R1, another R factor, R136drdH8, is derepressed in both K12 and S. typhimurium, so that the intervention of der is unnecessary for its derepression in the salmonella host.

Merinos (189) and Poll Dorsets (106) were compared for genetic variation at 30 loci for blood proteins. ‘Malic enzyme’ and NADH diaphorase I polymorphism occur in Merinos but not in Poll Dorsets, whereas both breeds are polymorphic for haemoglobin, erythrocyte X-protein, serum esterase, catalase and transferrin, although the breeds differ in the presence or absence of certain rare transferrin variants. Poll Dorsets but not Merinos have genetic variation of erythrocyte pyruvate kinase at low gene frequencies; Merinos but not Poll Dorsets have genetic variation of two erythrocyte Gly-Leu peptidases, glucosephosphate isomerase, superoxide dismutase, and NADH diaphorase II, all at low gene frequencies (P < 0·05).

Using Masatoshi Nei's (1972, 1976) standard genetic distance, over all 30 loci, to calculate the time of divergence of the two breeds, we obtained t = 69700 years – whereas sheep are believed to have been domesticated by man for not more than 11000 years, and ancestors of the British breeds and of the Merino have probably not been separated for more than 2000 years. Several possible explanations for this discrepancy are discussed, including the accuracy of the coefficient of codon change (α), changes in population size and structure, selection, and additional hybridization in the ancestry of the Merino.

X-ray-induced mitotic recombination within the lozenge locus of Drosophila melanogaster was found to be non-reciprocal. Recombination was detected by the presence of faceted spots in a smooth (lozenge) eye. Markers were present so that if recombination were reciprocal, equal numbers of vermilion and apricot-vermilion-coloured faceted spots would be formed. Of 19 faceted spots found among more than 60000 eyes examined, 10 were vermilion, 7 variegated (some vermilion and some apricot-vermilion-coloured facets), and 2 probably variegated. None was uniformly apricot-vermilion in colour. Four mechanisms for the formation of faceted spots are discussed: double reciprocal recombination, misrepair or gene conversion before chromatid replication, misrepair or gene conversion after chromatid replication, and misrepair or gene conversion followed by chromosome loss. The evidence most strongly supports the hypothesis that all faceted spots were formed by either misrepair following X-irradiation or gene conversion and were originally vermilion in colour. Subsequent chromosome loss from these vermilion cells led to the production of variegated spots. Variegated spots were generally smaller than those uniformly vermilion in colour, indicating that chromosome loss may occur with greater frequency in older irradiated larvae.

The sensitivity pattern of the Drosophila testis to TEM was analysed by means of a dual-purpose strain that allows the scoring of induced crossovers and sex-linked lethals in the progeny of the same flies. It was found that TEM produces the highest frequency of mutations in spermatocytes or late spermatogonia, while early spermatogonia are even less sensitive than mature spermatozoa. The discrepancy between this conclusion and that obtained by Fahmy & Fahmy (1955) is attributed to a difference in the method of analysis. The sensitivity pattern of the Drosophila testis to TEM resembles that to mustard gas and differs from that to X-rays. The sensitivity pattern of the mouse testis to TEM differs from that of the Drosophila testis.

The DNA structures around the G6PD coding region in three high-G6PD activity mutants and their low-activity revertants of Drosophila melanogaster were analysed by Southern blot using a cloned G6PD gene as a probe. As a result, two kinds of insertion sequences were found; one was present just 5′ to exon I (Ins1), and the other within the intron (Ins2). The Ins1 sequence was 3·5 Kb in two mutants and 2·9 Kb in one mutant. In both cases, it consisted of a core sequence either 1·2 or 0·6 Kb long flanked by terminal repeats. On the other hand, low-activity revertants possessed either a defective Ins1 or no Ins1. The Ins2 sequence was found in all mutants and revertants, but not in Canton S. Although a recombinant phage carrying the DNA fragment spanning the entire Ins1 has not been obtained, sequencing data of the clone containing only the terminal repeats demonstrated that the repeats are defective P elements. Comparison of the genomic DNA structures of mutants and revertants suggested that the element responsible for the positive regulation of the G6PD gene in the mutants would probably be the core sequence, but not the flanking defective P elements. It was also conjectured that the 1·2 Kb core sequence might be composed of two identical elements, which might transpose independently.

By the use of appropriate strains of Escherichia coli, Shigella flexneri and Salmonella typhimurium with and without an R factor, R100, the mechanism of ‘curing’ of R factor by acridine dyes was examined. This R factor was shown to confer increased sensitivity to acriflavine upon the host cells. E. coli strain W-3630, once infected with R100, has never been observed to segregate R− cells. When mixtures of R+ and R− cells of this strain were grown in acriflavine broth, the proportion of R− cells increased and was also correlated with the proportion in the initial inoculum. Other bacterial strains carrying R100 segregate R~ cells spontaneously. Growth tests starting with varying proportion of R+ and R− cells of these strains in acriflavine broth also gave a marked correlation between the initial and final proportions of R− cells, and indicated that the main cause of ‘curing’ the R factor was the selective enrichment of R− segregants present in the initial inocula or arising spontaneously during growth of the R+ culture. These results suggest that the mechanisms underlying the ‘curing’ of F and R factors are different. Tests with several acridine dyes gave results similar to those with acriflavine.

A low activity mutant of glucose-6-phosphate dehydrogenase, G6pda-m1Neu has been used to position G6pd in the mouse X chromosome. Linkage tests with tabby, Ta and harlequin, Hq, indicate a likely gene order of Hq–G6pd–Ta. Muscular dystrophy, mdx, has been located by two-and three-point crosses using Hprt, Pgk-1 and Moblo and suggest a gene order of Hprt–mdx–Pgk-1–Moblo. Together with existing linkage data a tentative order for the seven loci is Hq–Hprt–G6pd–mdx–Ta–Pgk-1–Moblo. The relative positions of G6pd and mdx have not been directly tested and G6pd is assigned provisionally proximal to mdx. In the three point test using Hq, G6pd and Ta the recombination frequency found between Hq and Ta was 9·9 ± 2·6%, substantially less than the value of 20·5 ± 2·1% reported by Isaacson et al. (1974).

We would like to use maximum likelihood to estimate parameters such as the effective population size Ne, or, if we do not know mutation rates, the product 4Neμof mutation rate per site and effective population size. To compute the likelihood for a sample of unrecombined nucleotide sequences taken from a random-mating population it is necessary to sum over all genealogies that could have led to the sequences, computing for each one the probability that it would have yielded the sequences, and weighting each one by its prior probability. The genealogies vary in tree topology and in branch lengths. Although the likelihood and the prior are straightforward to compute, the summation over all genealogies seems at first sight hopelessly difficult. This paper reports that it is possible to carry out a Monte Carlo integration to evaluate the likelihoods pproximately. The method uses bootstrap sampling of sites to create data sets for each of which a maximum likelihood tree is estimated. The resulting trees are assumed to be sampled from a distribution whose height is proportional to the likelihood surface for the full data. That it will be so is dependent on a theorem which is not proven, but seems likely to be true if the sequences are not short. One can use the resulting estimated likelihood curve to make a maximum likelihood estimate of the parameter of interest, Ne or of 4Neμ. The method requires at least 100 times the computational effort required for estimation of a phylogeny by maximum likelihood, but is practical on today's work stations. The method does not at present have any way of dealing with recombination.

For one-, two- and n-locus models of a quantitative trait assumed to be determined by overdominant loci, it is shown that the mean of an inbred line will be equal to or larger than the mean of the base population if the original gene frequencies satisfy a condition which is generally a function of the degree of overdominance and of the genotypic values.

In Drosophila melanogaster a large number of the genes coding for 18S and 28S rRNA are interrupted in the 28S region by insertions of two types. Ribosomal insertion transcripts were compared in wild-type and bobbed strains. We found that the level of insertion transcripts increased in bobbed mutants after deletion of 50% of INS− genes, and inversely decreased in revertants when more than 50% of wild-type levels. Among type II insertion transcripts we found a predominant 3·5 kb RNA, precisely of the most frequent insertion size. No primary insertion transcript has been found, although it could be undetected if very fast splicing leads to mature 28S occurs.

Genomic patterns of occurrence of the transposable element hobo are polymorphic in the sibling species Drosophila melanogaster and D. simulans. Most tested strains of both species have apparently complete (3·0 kb) and smaller hobo elements (H lines), but in both species some strains completely lack such canonical hobo elements (E lines). The occurrence of H and E lines in D. simulans as well as in D. melanogaster implies that an hypothesis of recent introduction in the latter species is inadequate to explain the phylogenetic occurrence of hobo. Particular internally deleted elements, the approximately 1·5 kb Th1 and Th2 elements, are abundant in many lines of D. melanogaster, and an analogous 1·1 kb internally deleted element, h del sim, is abundant in most lines of D. simulans. Besides the canonical hobo sequences, both species (and their sibling species D. sechellia and D. mauritiana) have many hobo-hybridizing sequences per genome that do not appear to be closely related to the canonical hobo sequence.