Ca and P metabolism in the grey-lethal mutant mouse has been investigated. This animal is hypocalcaemic and hypophosphataemic and the serum alkaline phosphatase is elevated far above the normal. Increased bone ash content has been attributed to an elevated bone Ca. From in vitro experiments involving steady-state distributions of calcium and phosphate it is concluded that active bone metabolism is reduced in mutant bone. This reduced ratio may be attributed to an increased passive ion solubility.

These results tend to the assumption of an hormonal imbalance in this mutant system. An increased production of thyrocalcitonin has been postulated to account for these findings.

Esterase-27A (ES-27A) was characterized in strain A/WySnA by a cascade of seven bands seen after disc electrophoresis of serum and subsequent staining for esterase. ES-27A catalyses the hydrolysis of thiocholine butyrate and is strongly inhibited by 100 μm tetraisopropyl pyrophosphamide (isoOMPA). Hence, the enzyme was concluded to be a cholinesterase EC 3.1.1.8. A heat-labile form termed ES-27B was represented by strain AKR/Han. From a three-point cross (AKR/Han, A/Wy) and a five-point cross (AKR/Han, SEG/1), the gene order on chromosome 3 was concluded to be centromere–Car-2–Es-26–Es-27–Amy-1–Adh-1.

Wright first introduced the idea that random genetic drift and classical mass-action selection might combine in such a way as to allow populations to find the highest peak in complicated adaptive surfaces. His theory assumes large but structured populations, in which mating is spatially local. If gene flow is sufficiently low, and the subpopulations (demes) are small enough, they will be subject to genetic drift. Distant demes drift independently, allowing many independent searches of the adaptive surface to take place. A deme that has shifted to a higher peak can, by emigration, cause the rest of the demes to shift to the higher peak. The probability of this shift depends on the migration rate. Previous studies have concluded that very little migration is necessary to effect the shift in adaptive peaks that characterizes the last phase of Wright's Shifting Balance Process (SBP).

Here we present the results of a computer study that investigates the roles of dispersal distance, the degree of epistasis in the fitness surface, and recombination on the shifting balance process. In particular, we measure their effect on the population's mean fitness. We show that over a range of dispersal distances the advantage of the SBP is a monotonically increasing function of the amount of epistasis. Our results show that the extent of dispersal that results in the greatest effect of the SBP in increasing mean fitness depends on the extent of epistasis. Finally, for low levels of epistasis, higher recombination performs better, while for intermediate levels, lower recombination results in a greater advantage of the SBP.

Sixty-six individual tests on an array of skeletal variants showed an essential absence of parent-offspring correlations in the inbred strains C57BL, A and CBA in the mouse. It is concluded that these strains, and inbred strains of mice in general, are genetically homogeneous except for the differentiation of genetically distinct sublines as the result of mutations.

1. Two methods are examined of introducing new genetic variance into a line of mice selected for high 6-week weight which, at its limit, displayed no additive genetic variance.

2. The first method—irradiation—gave largely negative results. Any further gain under selection that was achieved could not be clearly distinguished from a possible environmental trend.

3. The second method—outcrossing to an unselected strain and then selecting from the cross—resulted in a clear gain over the original limit, but nine generations were required even to recover the original limit.

4. Various methods of transcending selection limits are evaluated in terms of their application to livestock improvement.

Contrary to the conclusion of earlier workers, penetrance of a very rare genetic defect, congenital tremor in White Leghorn chicks, was found to be complete. By appropriate correction of the original data for small family size it is shown that the defect is determined not by one but two pairs of autosomal recessive genes. In the terminology of human genetics, ascertainment of affected individuals corresponded to conditions of ‘truncate’ selection in the case of maternal sibships and more nearly to ‘single’ selection in the case of paternal sibships.

Linkage disequilibrium between five polymorphic enzymic loci of the third chromosome (Esterase-6, Phosphoglucomutase, Esterase-C, Aldehyde Oxidase and Acid Phosphatase) was studied in experimental populations of Drosophila simulans. Gametic data were obtained by mating sampled males with homozygous females at the five loci. Four cage populations were initiated with flies caught from natural populations. Extensive linkage disequilibrium was detected after 25 or 34 generations. The effective size of these populations was estimated about 400. Monte-Carlo simulations were performed in order to determine whether the observed disequilibria could be due to genetic drift. The observed probability distribution of the experimental values of r (the gametic correlation coefficient) was consistent with the distribution expected under random genetic drift. Our results are thus in accordance with the neutralist hypothesis.

The effect of dietary supplements of individual l-amino acids on the expression of the eyegone and eyelessK mutants of Drosophila melanogaster are compared. In both mutants, eye size is reduced by excess levels of tryptophan, phenylalanine and methionine, and in each case the effects are independent of metabolic competition for pyridoxal phosphate. A dietary interaction involving methionine and UNA can be demonstrated in the eyK strain, but the mechanism of action of this amino acid is obscure. Tryptophan metabolism is examined in detail. Although both tryptamine and serotonin have significant effects, the action of tryptophan on eye development is largely independent of its metabolic products. Conversely, the effect of dietary supplements of certain catecholamines is consistent with the action of phenylalanine. The action of certain metabolic inhibitors provides additional support for the suggestion that the catecholamines have an important effect on morphogenesis in the eye imaginai disks. Eye development is also affected by increasing concentrations of γ-amino-butyric acid, and this, taken together with the effect of the catecholamines and indolalkylamines, suggests that physiological control of the action of the mutant genes on eye development involves a group of compounds characteristically associated with nervous tissue. Eye development in the eyK strain may be influenced by the availability of acetyl CoA, which would be expected to affect acetylcholine biosynthesis. Possible mechanisms of action of the effective dietary treatments are discussed, together with a tentative hypothesis regarding the mode of action of the mutant genes on eye development.

It is known that under neutral mutation at a known mutation rate a sample of nucleotide sequences, within which there is assumed to be no recombination, allows estimation of the effective size of an isolated population. This paper investigates the case of very long sequences, where each pair of sequences allows a precise estimate of the divergence time of those two gene copies. The average divergence time of all pairs of copies estimates twice the effective population number and an estimate can also be derived from the number of segregating sites. One can alternatively estimate the genealogy of the copies. This paper shows how a maximum likelihood estimate of the effective population number can be derived from such a genealogical tree. The pairwise and the segregating sites estimates are shown to be much less efficient than this maximum likelihood estimate, and this is verified by computer simulation. The result implies that there is much to gain by explicitly taking the tree structure of these genealogies into account.

We conducted classical genetic analysis of the difference in male genitalia and hybrid sterility between the island-dwelling sibling species Drosophila sechellia and D. mauritiana. At least two loci (one on each autosome) are responsible for the genital difference, with the X chromosome having no significant effect. In contrast, male hybrid sterility is caused by at least four gene loci distributed among all major chromosomes, with those on the X chromosome having the largest effect.

We also show that the large difference in ovariole number between D. sechellia and its mainland relative D. simulans is due to at least two gene substitutions, one on each major autosome. The X and the left arm of the second chromosome, however, have no significant effect on the character. This implies that the evolution of reduced ovariole number involved relatively few gene substitutions.

These results extend previous findings that morphological differences between Drosophila species are caused by genes distributed among all chromosomes, while hybrid sterility and inviability are due primarily to X-linked genes. Because strong X-effects on male sterility have been found in all three pairwise hybridizations among D. simulans, D. sechellia and D. mauritiana, these effects must have evolved at least twice independently.

Methods for estimating probability of identity by descent (f) are derived for data on numbers of genotypes at single loci and at pairs of loci with many alleles at each locus. The methods are general, but are specifically applied to data on genotype frequencies in zygotes of the malaria parasite sampled from its mosquito host in order to find the extent of outcrossing in the parasite and the degree of clonality in populations. It is assumed that zygotes are the outcome either of gametes of the same clone, in which they are identical at all loci, or are products of two random, unrelated clones. From the estimate of f an effective number of clones per human host can also be derived. For Plasmodium falciparum from a Tanzanian village, estimates of f are 0·33 from data on zygote frequencies at two multiallelic loci, indicating that two-thirds of zygotes produce recombinant types.

The recessive mutant pudgy in the mouse has a greatly shortened vertebral column with highly irregular fusions between vertebrae and fragments of vertebrae. Ribs and sternum are also involved, but the rest of the skeleton is quite normal. The deformities arise from a defective segmentation. Although the paraxial mesoderm forms somite tissue with an epithelially arranged outer layer, this material either shows only an abortive segmentation into somites or, in the tail, none at all. A belated segmentation into dermomyotomes ultimately takes place, but the sclerotomic material remains continuous and gives rise to erratically abnormal blastemata which then chondrify and ultimately ossify.

1. Five additional phenylalanine (PHE)-requiring mutants have been isolated but they do not add to the number of loci already known which have been designated phenA (phen2 and its alleles) and phenB (phen6).

2. Two pathways for tyrosine (TYR) synthesis in A. nidulans have been proposed: the well-known one by the transamination of p-hydroxyphenylpyruvic acid and an alternative one, as in animals, by the hydroxylation of PHE.

3. Ten allelic partial TYR-requiring mutants (tyrA), presumably blocked in the transamination pathway, have been isolated after N-methyl-N′-nitro-N-nitrosoguanidine (NTG) treatment of bil;phenA3 conidia.

4. Four partial TYR requirers (at another locus—tyrB) have been isolated after NTG treatment of tyr A7, bi1 conidia. They are presumably blocked in an alternative pathway for TYR synthesis, i.e. in the PHE-hydroxylation pathway.

5. tyrA mutants have been found to be p-fluorophenylalanine (FPA)-resistant and allelic to mutants at the fpA locus. tyrB mutants have been found to be very leaky and FPA-sensitive. tyrA;tyrB double mutants have been found to be exacting TYR requirers.

6. Mutants at loci fpA (tyrA) and fpE (anthranilic acid-requiring) have been interpreted to be p-fluorophenylalanine-resistant due to an oversynthesis of PHE.