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 genetic relationships of the available second chromosome melanotic tumour mutants in Drosophila melanogaster have been investigated. Complementation tests demonstrate the existence of new alleles of the tu bw locus and show that tu-W and tu-g are alleles. The data suggest that there is a minimum of three major gene loci on the second chromosome involved in tumorigenesis. A number of modifier genes were found which affect the penetrance of the major tumour genes analysed. These and the problems they cause in mapping the low penetrant tumour genes are discussed. It has not been possible to map tu-48a, tu- W and tu-g accurately, due largely to the presence of modifier genes. It appears that the genetic basis for melanotic tumour formation is complex.

When a selectively favourable gene substitution occurs in a population, changes in gene frequencies will occur at closely linked loci. In the case of a neutral polymorphism, average heterozygosity will be reduced to an extent which varies with distance from the substituted locus. The aggregate effect of substitution on neutral polymorphism is estimated; in populations of total size 106 or more (and perhaps of 104 or more), this effect will be more important than that of random fixation. This may explain why the extent of polymorphism in natural populations does not vary as much as one would expect from a consideration of the equilibrium between mutation and random fixation in populations of different sizes. For a selectively maintained polymorphism at a linked locus, this process will only be important in the long run if it leads to complete fixation. If the selective coefficients at the linked locus are small compared to those at the substituted locus, it is shown that the probability of complete fixation at the linked locus is approximately exp (− Nc), where c is the recombinant fraction and N the population size. It follows that in a large population a selective substitution can occur in a cistron without eliminating a selectively maintained polymorphism in the same cistron.

Mutants of Saccharomyces cerevisiae whose colonies were blue when grown on nutrient agar medium containing methylene blue reverted to wild-type with white-colony phenotype at high frequency. This reversion was controlled by nuclear gene suppressors in some mutants, and by cytoplasmic suppressors in others. Each of the latter suppressed several independetly segregating blue mutants. These suppressors could be divided into two classes: suppression by petite mutations which behaved as recessives, and suppression by a cytoplasmic factor in respiration-sufficient cells which behaved as dominant over wild-type but might also be a mutation of rho. A relationship between blue mutation and temperature sensitivity was suggested.

The amino acid analogues p-fluorophenylalanine (PFP) and ethionine (ETH) are strongly mutagenic in Coprinus lagopus. The most pronounced effect was found with suppressor mutations of the met-1 locus. PFP, at a concentration of 2·4 × 10−4 M, increased the mutation frequency 500 fold and ETH, at a concentration of 2·4 × 10−3 M, 30 fold over the spontaneous mutation frequency. From the spectrum of suppressors of the met-1 locus and the dominant revertants of the ad-82 locus, induced by analogue treatments, it was concluded that both analogues induce single base-change mutations. The dose response curves follow a sigmoid plot, revealing that within a certain range of analogue concentrations, muta-genesis is strongly dose dependent.

Using analogue resistant mutants, it has been shown that PFP mutagenesis is a function of its incorporation into protein. However, ETH mutagenesis is independent of protein incorporation but can be correlated with the degree of ethylation of nucleic acids. The synergistic effect PFP and ETH supports the evidence of the different mutagenic actions of the two analogues.

Techniques for isolating and analysing temperature-sensitive mutations in Habrobracon serinopae are presented. The temperature-sensitive patterns and lethal phases are described for nine different mutant strains. Such mutants are well suited for the study of gene action during development.

Methods have been developed for the selection of mutants resistant to p-fluorophenylalanine, chloramphenicol and actidione. Resistance to p-fluorophenylalanine and to chloramphenicol was inherited as if determined in each case by a single dominant allele present in diploid somatic nuclei. Inheritance of mating type was anomalous in crosses involving drug-resistant mutants. Presumptive mating-type heterokaryons were generated in a few per cent of sexual progeny from a wild-type cross.

A selective procedure is described for the isolation of deletions in phage T4. This is based on the properties of partial diploids which possess a tandem duplication covering the rII region. The starting-point of the procedure is a particular s1231/3157 diploid which has a high segregation frequency and so possesses a long duplication. The replacement in this diploid of the large deletion 3157 by the small one 196 further increases the length of this duplication and removes the terminal redundancy of the resulting phage which are then non-viable. New compensating deletions which restore the terminal redundancy and thus the viability to these diploids are thereby selected. Nine new independent T4 deletions have been isolated by this procedure. The length of three has been estimated by terminal redundancy measurements and each found to be appreciably longer than the rII region. While developing the isolation procedure a key diploid intermediate was identified with the property that is was completely stable; that is, unlike typical diploids which continually generate haploid segregants during phage multiplications, this diploid strain produced no viable haploid segregants. This unexpected finding led us to examine the general problem of how tandem duplications can be stabilized. The solution we propose here is a structural one involving new stabilizing deletions which penetrate into one arm of the duplication removing certain essential genes. These stabilizing deletions are located in such a way that all haploid segregants formed by recombination are necessarily non-viable. Further investigations of the original stable diploid, and others isolated subsequently, validated this model for these phage diploids. It also led to the recognition of several novel genetic structures involving repeated DNA sequences which, together with the concept of the stabilizing deletions, could be of general significance.

In the preceding paper (Van de Vate & Symonds, 1974) a deletion, sdl, has been reported that stabilizes an rII diploid by penetrating into the region of the duplication from the right-hand side (if we take the rIIB gene located to the right of rIIA). Here we wish to report on a different stabilizing deletion, sd2. Evidence will be presented in favour of penetration of the duplication from the left-hand side. The right-hand terminus of the deletion is located within the rIIA gene.

A technique is reported for crossing strains of Aspergillus nidulans which produces hybrid cleistothecia in 7 days. The method depends on the partial inhibition of cleistothecium formation of auxotrophic mutants by growth-factor limitation. Cleistothecia form at the junction of two strains inoculated on to complete medium. The method has a number of advantages over standard techniques.

Wild-type cells of Aspergillus nidulans have undetectable NADL-glutamate dehydrogenase activity when utilizing glucose and high levels of NAD L-glutamate dehydrogenase when utilizing certain amino acids as sole carbon sources.

A mutant, designated gdhCl, has appreciable NAD-GDH activity when utilizing glucose as a carbon source. The gdhC1 mutation is semi-dominant and is located in linkage group III.