Nuclear DNA syntheses have been measured microspectrophotometrically in course of meiotic nuclear development in Neurospora crassa. The purpose of the study has been to establish the timing of these DNA syntheses in relation to meiosis and in the formation of its final products in an ideal genetic material, where the products of the meiotic division can be recovered and identified. Spectrophotometric analysis has indicated that the last premeiotic DNA replication is completed before caryogamy; a postmeiotic DNA replication takes place at the tetrad of the nuclei level; and finally a second postmeiotic DNA replication occurs in the ascospores to result in eight binucleated ascospores. The timing of postmeiotic replication is compatible with the models explaining gene conversion through the postulated mechanisms involving heteroduplex formation.

The model of random selection coefficients is considered in the context of a finite population of diploids. The selection coefficients of the homozygotes are allowed to vary with equal variance while the fitness of the heterozygote is kept fixed. Steady-state solutions are found in the case of equal two-way mutation rates with particular reference to the expected heterozygosity. Increasing the variance of the selection coefficients of the homozygotes is found to uniformly increase the heterozygosity for all values of the average selection coefficients and its effect is largest when the selection coefficients of the homozygotes are fully correlated. The fate of mutant genes is also considered in the case of random selection coefficients by looking at the probability of ultimate fixation and the mean times to fixation and extinction. The errors in previous calculations (e.g. Kimura, 1954; Ohta, 1972) are pointed out. It is found that a small average heterozygote advantage together with a reasonable degree of variance in the coefficients can cause an unexpectedly large amount of heterozygosity to be maintained. It is also seen that probabilities of fixation and mean times to boundaries are usually increased by increasing the variance showing that it in fact helps to keep the population heterozygous for much longer than the non-random case. This is in contradiction to some conclusions of Karlin & Levikson (1974) because their haploid results are not easily extendable to the consideration of this sort of diploid model.

A technique for obtaining bryozoan chromosome spreads is described. Karyotypes were prepared for the following phylactolaemate species: Plumatella emarginata, 2n = 14; Hyalinella punctata, 2n = 14; Fredericella sultana, 2n = 14; and Pectinatella magnifica, 2n = 18. Approximate numbers were obtained for Lophopodella carteri, 2n 18–22, and three ctenostomes, Pottsiella erecta, 2n = 22 or 24; Amathia semiconvoluta, 2n about 30; and Paludicella articulata, 2n about 20. Differences between the bryozoan karyotypes seen in this study correlate with taxonomy.

For a model in which quantitative traits are assumed to be determined solely by additive genes at many loci, formulae are developed for the variance among replicated small populations of size N, maintained without selection, of the additive genetic variance, heritability, genetic correlations and similar parameters. The base population is assumed to be in linkage equilibrium, but it is argued that most of the variation in the within-line additive variance (VAt at generation t) is due to linkage disequilibrium caused by sampling. If is the squared correlation of gene frequencies averaged over all pairs of loci at time t, the coefficient of variation (CV) of VAt equals , with similar formulae for other parameters.

The formulae are evaluated for models of loci distributed uniformly along the chromosome but much of the disequilibrium is due to loci on different chromosomes. For unlinked loci CV(VAt) reaches √4/(3(N)), and for mammalian models, this value is not greatly exceeded. The variance in successive generations has a correlation of at least one-half due to the maintenance of linkage disequilibrium. The magnitude of this variance in parameters and their autocorrelation with time shows that accurate predictions cannot be made about genetic parameters in the base population from single replicate results.

A population with N monoecious individuals, and having two alleles, is considered. The problem of calculating the fixation probability of a particular allele under random fluctuation of selection intensities is re-examined, employing finite Markov chain methods. An approximate but general expression for this probability is obtained and the results obtained by previous workers are shown to be special cases of this result.

Inositol independent (inl+) strains were obtained either as transformants following treatment of the inositol requiring (inl) strains of Neurospora crassa with the wild-type DNA or as revertants without any DNA treatment. A significant number of the inositol-independent transformants were also found to have acquired additional mutations called osmotics (os) which made them unable to grow on 1 m-NaCl medium. None of the inositol-independent revertants were found to possess such osmotic mutations and their growth remained unaffected by the presence of NaCl. Many of the osmotic mutants described here were found to be new alleles of the previously known os–1 mutation on the linkage group I of Neurospora crassa. The remainder were found to map at two new genetic loci designated as os-6 and os-7; these loci were found to be closely linked to os–1. Among the new osmotic mutants only os-1 and os-6 mutants showed intragenic complementation. The mechanism of DNA-induced mutation during transformation is discussed.

Plasmodium formation in the Myxomycete Physarum polycephalum normally involves fusion of haploid amoebae, carrying different alleles at the mating type (mt) locus, to give diploid plasmodia. Strains carrying the mth allele are capable of undergoing the amoebal–plasmodial transition with high efficiency within amoebal clones, resulting in the formation of haploid plasmodia. NMG mutagenesis of mth amoebae, followed by an enrichment procedure, was used to isolate mutants in which such clonal plasmodium formation was either delayed or absent. Thirteen mutants of the second type were analysed. Three of these were temperature-sensitive for plasmodium formation. All thirteen mutants were able to form diploid crossed plasmodia when mixed with a mt1 strain. Three new genes were identified and designated npfA, npfB and npfC. A mutant allele of npfA rendered clonal plasmodium formation temperature-sensitive, but did not prevent crossing at the non-permissive temperature with derived strains carrying the same mutant allele. No recombination was detected between npfB or npfC and mt, but npfA was unlinked to mt and a locus (apt-1) shown in a previous study to be involved in plasmodium formation. The genes npfB and npfC were distinguished by complementation analysis. Strains of the genotype npfB−; npfC+ behaved in the same way as strains carrying the mt2 allele. The nature of the mutants and the role of the mating-type locus in the initiation of plasmodium formation are discussed.

Females from an Indian wild population of Aedes aegypti were crossed to males carrying the sex ratio distorter factor MD which shows meiotic drive. Progenies from F1 males were tested for sex ratio distortion, i.e. the chromosomes from the wild females were screened for their resistance to the action of MD. The distribution of sex ratio in the progenies of different F1 males indicated a polymorphism in the wild population for resistant and sensitive variants of the X chromosome. Seven discrete categories of X appear to exist, associated with sex ratios ranging from 50% ♀ to less than 1·25% ♀. The overall level of resistance varied slightly but significantly in different parts of a town. The results are discussed in relation to the use of sex ratio distortion for genetic control of mosquitoes.

Wild populations of the Norway rat, Rattus norvegicus, in Jutland have been known to be resistant to the anticoagulant rodenticide warfarin since 1962. The inheritance of the resistance was investigated in the F1, backcross and intercross. The results are consistent with the resistance being due to a major gene at the Rw locus. Resistant homozygotes, heterozygotes and susceptible homozygotes appeared to be distinguishable experimentally on the basis of differences in their susceptibility to vitamin K deficiency. The results are discussed in relation to previous studies of the inheritance of warfarin resistance in rats.

We have shown in an earlier paper that there is routinely a large correlation between the heterozygosity of common (P > 0·05) alleles and the number of rare (P ≤ 0·05) alleles at allozyme loci in Drosophila. We postulated that this correlation might be due to a high rate of intragenic recombination. While these correlations are large enough to be significantly different from zero, their relation to the mean correlations expected under the neutrality models is unknown. This paper reports the findings of a computer analysis determining the correlation for neutral allele pools as specified by the infinite-allele and charge-state models.

In the analysis, mean correlations for a range of Neμ values and sample sizes of 100 and 1000 genes varied from a high of 0·284 to a low of – 0·780. For the particular values of Neμ relating to the heterozygosity of Drosophila allozymes in natural populations, tests of the empirical correlations to the means expected under the neutral models are made. Most empirical correlations are significantly different from the mean correlations under the neutrality models.

R388s is a mutant of the R factor, R388. Unlike its parent R388s does not confer trimethoprim resistance, though it does confer sulphonamide resistance and the ability to transfer. It is shown that when bacteria harbour R388s mutations to trimethoprim resistance occurred at a high frequency (3·5 × 10−4), whereas such mutations never occurred when the host lacked the R factor. Bacteria harbouring R388s did not mutate to resistance to any other antibiotics at a detectable frequency.

The expression of trimethoprim resistance in bacteria possessing R388s appears to require two genes, one located on the R factor and the other situated presumably on the chromosome. The mechanism of trimethoprim resistance in these bacteria is probably due to reduced permeability and is thus quite unlike the insusceptible target site mechanism of the parent R factor, R388.

Mice were selected for high and low body weight at 5 and at 10 weeks of age. Selection was performed (1) separately for each trait, and (2) for various combinations of the two traits, using (a) independent culling levels and (b) restricted indices. Two-way selection for each trait separately gave large responses and correlated responses. Selection by independent culling levels intended to increase 5-week weight while restricting change in 10-week weight gave no demonstrable response; selection by culling levels intended to decrease 5-week weight while restricting change in 10-week weight resulted in decreases in body weights at both ages. Index selection, intended to change weight at one age while holding that at the other age constant, was generally successful. Observed responses did not conform very well with predicted responses for either index or culling levels selection. The significance of these observations in regard to the problem of selection involving restriction of traits is discussed.

Mutants with abnormalities which were the consequence of the formation of haematomas during gestation were designated as ‘foetal haematomata’ (fh). The fh homozygotes were found to be morphologically and embryologically very similar to myelencephalic bleb (my) mice. It was also found, however, that the fh and my mutants were separate genetic entities due to two independently segregating recessive genes.

The prophage of the phage B3 of P. aeruginosa exhibits superinfection inhibition towards certain R plasmids such as R18-1 or R18-3 as shown by a severe depression (c. 10−6) in the conjugal transfer of these plasmids into B3 lysogens. The transfer of other R plasmids into such lysogens and the transfer of R18-1 or R18-3 into bacteria lysogenic for unrelated phages was unimpaired. R18-1 or R18-3 was non-transducible into B3 lysogens although transducible into non-lysogens. The interaction appeared to be reciprocally expressed since B3 lysogenization of bacteria R+ for R18-1 or R18-3 was also reduced. Consistent with the failure of co-existence of the prophage and the plasmids was the observation that when the transconjugants from the cross R18-1 donor ×B3 lysogenic recipients were tested, transfer-deficient plasmid derivatives were encountered (about 40%). Other transconjugants were cured of prophage, or carried mutant B3 prophage with lytic, lysogenization or superinfection inhibition functions impaired.

A second chromosome of Drosophila melanogaster (symbol 31.1) isolated from a natural population of North-Western Peloponnesus (at a distance of 8 km from the city of Patras) was found to induce recombination in heterozygous males, both in the second and third chromosomes. The present study also revealed the following points. (1) The phenomenon is temperature-sensitive with higher male recombination at 29 °C than at 25 or 15 °C. (2) The temperature-sensitive period is during the larval stage where premeiotic divisions of germ cells take place. (3) Suppression of male recombination in both the second and third chromosomes occurred when 31.1/CyL4 females were used in the matings, and (4) the suppression of male recombination is caused by a cytoplasmic factor of the CyL4/Pm stock.

The homothallic amoebal clones of Physarum polycephalum are of potential use in understanding the developmental genetics of this organism. Such an application requires that complementation and recombination analysis be possible between pairs of homothallic clones. This paper is a report of the formation of mixed plasmodia by pairs of homothallic amoebal clones. In order to detect such mixed plasmodia use was made of two marker genes involved in plasmodial fusion, fusA and fusB. Sporulation of a mixed plasmodium formed from two homothallic (delayed) amoebal clones yielded progeny amoebae which were genetically recombinant. It is deduced from the ratios of various genotypes in these progeny clones that the mixed plasmodium was diploid and that meiosis was associated with sporulation. There is therefore no impediment to the use of the homothallic strains for genetical analysis. The progeny amoebal clones were observed to be showing segregation for the characters homothallic (rapid) and homothallic (delayed). This observation, taken together with other related observations, suggests that the homothallic (delayed) character is produced by mutation of the homothallic (rapid) character. The rare plasmodia formed by a homothallic (delayed) amoebal clone are the result of reversion of this mutation. Amoebal clones of the homothallic (delayed) type are therefore developmental mutants unable to perform the differentiation from amoeba to plasmodium.

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.

Cell lineage analysis of the maroon-like mutation of Drosophila melanogaster revealed the most extensive degree of non-autonomy reported to date in Drosophila: all 1454 gynandromorphs in which X chromosome loss uncovered the ma-l mutation had ma-l+. eye colour. In contrast, among 331 gynandromorphs in which X chromosome loss simultaneously uncovered the vermilion and maroon-like mutations, approximately 16% had v phenotype but with one possible exception all gynandromorphs again had ma-l+ eye colour. These results suggest that very small amounts of the ma-l+ gene product are necessary for wild-type eye colour development and they are therefore compatible with the one cistron–allelic complementation model that has been proposed for the ma-l locus. They also provide the best estimate available to date of In(1)wvc-induced internal mosaicism: 7%. A preliminary attempt to detect DNA-induced transformants among 6 DNA-injected preblastoderm ma-l embryos and at least 80000 of their F1 to F4 descendants has yielded completely negative results. An investigation of the maternal effect which ma-l+ mothers exert on the eye colour of their genetically ma-l offspring revealed that, in contrast to earlier observations, this effect is not universal: some phenotypically ma-l and intermediate ma-l flies were observed in young cultures. The discrepancy between this and earner observations is probably attributable to as yet uncharacterized nutritional deficiencies in the diet of flies used in this experiment. Cytoplasm drawn from blastoderm ma-l+ embryos and injected into the posterior region of ma-l preblastoderm embryos failed to induce eye-colour alterations in all seven flies which survived the treatment. Injection of the contents of embryos of certain genotypes and developmental stages into ma-l pupae 24–48 h old did alter in some instances the eye colour of treated ma-l flies. Various tests strongly suggest that these alterations are not due to injection of a substance that has been stored in the egg during oogensis or that has been produced by the embryo itself prior to injection and they therefore preclude the possibility that a simple in vivo bioassay for the ma-l+ substance has been achieved. Rather, they indicate that the observed eye-colour alterations are due to transplantation of blastoderm-stage embryos which remain active long enough within ma-l hosts to produce and release a substance into the hosts' haemolymph and that this substance in turn induces phenotypic alterations in the hosts' eye colour. When v and ma-l eye colour changes are simultaneously monitored, it appears that injection of embryonic contents into pupae is equally or more effective in modifying the v phenotype than in modifying the ma-l phenotype. Based on these observations, a tentative hypothesis regarding the time of activation of the ma-l+ gene and the relationship between the immediate product of this gene, the maternal substance stored in the egg and the substance released by tissue transplants is proposed.

A total of 39 mutants at the grey-3, grey-4 and grey-5 spore colour loci in Sordaria brevicollis have been investigated for conversion pattern by crossing them with wild type and counting aberrant asci. Twenty-one of the mutants were obtained with ICR170 and all showed postmeiotic segregation only rarely (0–8% of the aberrant asci); two showed conversion predominantly to wild type (class A) and the other 19 predominantly to mutant (class B). Six mutants were obtained with ethylmethane sulphonate and one with nitrosoguanidine, and they all showed postmeiotic segregation frequently (14–54% of the aberrant asci) and conversion usually about equally frequently in each direction, though with considerable diversity between mutants (class C). Eleven UV-induced mutants comprised one of class B and ten of class C. There was considerable variation in aberrant ascus frequency between alleles, but conversion pattern seemed to be independent of this frequency.

In order to test the feasibility of preservation, of genetic stocks of mice by storage in liquid nitrogen, mouse embryos at the 8-cell stage, were frozen and stored in liquid nitrogen at – 196 °C under increased radiation exposures of 1·8×, 9× and 84× background levels for periods of 6–8 months, 10–12 and 27–29 months, the 1·8 × level being regarded as a control. Their survival rates to the blastocyst stage, and after transfer to recipient females, to foetal or liveborn stages were then compared with those of unfrozen or short term frozen control embryos. The freezing process per se caused a marked loss of viability, in comparison with the unfrozen controls, but at the 1·8× radiation level there was then no further loss in viability even at the longest storage time (27–29 months). Similarly, at the 9× radiation level there was no loss of viability during storage up to 29 months, but at the 84× level the proportions of implanted embryos and live foetuses were slightly reduced. It was not clear if this was a true effect of radiation, since it was not related to time of storage. Considering all groups, about 20–30% of the embryos originally frozen were recovered as foetuses or liveborn young. It is concluded that the preservation of genetic stocks by storage in liquid nitrogen is a feasible proposition.