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.

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.

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.

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.

The t-haplotype t6 interacts with brachyury, T, to produce taillessness, and exhibits lethality, male sterility and high male segregation ratio. Mutant haplotypes derived from t6 which have lost the lethality also lose the sterility. We here report that two mutants which have retained the lethality have also retained the sterility and suggest that the two properties of lethality and sterility are due to a factor or region of the t-haplotype located close to the locus of tf. Although t6 has a high male segregation ratio, mutants derived from it may have low or normal ratios. In trans heterozygotes of two mutant haplotypes the ratios tended to be equalized, whereas in cis heterozygotes a high ratio like t6 was obtained, at least in one case. On this evidence the low-ratio gene Low is reinterpreted as a mutant t-haplotype and designated tlow. It is suggested that abnormal ratio is due to an A-factor or region located between the loci of T and tf, so that t6 carries T-, A- and LS-factors which can exist separately and retain their properties. t6 may extend less proximally than other natural t-haplotypes, which in general may involve changes in interstitial heterochromatin.

Systems for the detection of postmeiotic segregation in unordered octads are described for 4:4(2), 6:2(2), 2:6(2), 5:3(3), 3:5(3) and 4:4(4) segregations, where the number in parentheses is the number of pairs of non-identical sister-spores. Linkage relations, centromere distances and phenotypic detectability of suitable combinations of markers for initial selective identification of such segregations, and subsequent confirmation tests, are discussed; correction formulae are given to allow for non-detection of certain classes in particular circumstances. Using one such system in Ascobolus immersus, we detected 4:4(2), 6:2(2) and 2:6(2) segregations at the w-78 site: 2:6(2)s were previously unknown. Initial visual detection in this system was from octad phenotype ratios for w-78 (white ascospore) and gr-3 (granular ascospore pigmentation), with mating type and parafluorophenylalanine resistance as confirmatory markers after germination. Corresponding-site interference for wider ratio and – for the first time – narrower ratio unique classes was determined: it was moderately positive or moderately negative, depending on the cross and segregation class involved.

The recessive mutant gene downless (dl) causes abnormal texture of the coat and absence of hair on the tail. The dl locus had previously been shown to act in the epidermis and not in the dermis. To obtain evidence on the pattern of proliferation of epidermis, downless ↔ normal chimaeras were produced by embryo aggregation, and the pattern of normal and mutant hair in the coat was examined. The chimaeras showed a pattern of narrow transverse stripes of normal and abnormal hair. This pattern was similar to that found in mice chimaeric for alleles at the agouti locus known to act in the dermis. This evidence supports the conclusion that the pattern of cell proliferation is similar in dermis and epidermis, and is compatible with the hypothesis that both tissues proliferate by lateral coherent clonal growth from a randomly mixed array of longitudinally arranged cells.

The inheritance of reaction to halothane anaesthesia (so-called malignant hyperthermia syndrome) in pigs was studied in a series of 61 litters by 18 sires from an F3–F4 Pietrain–Hampshire crossbred population. A single locus two allele model allowing for reactors from all three genotypes, was fitted by maximum likelihood. It was concluded that the reaction is due to a single autosomal recessive gene with a frequency of 0·46 (0·44–0·48) and penetrance of 0·95 (0·92–0·98) in this stock.