5-Bromodeoxyuridine (BrdU)-resistant mutants of Physarum polycephalum were isolated as colonies of myxamoebae growing on BrdU-substituted bacteria after exposure to long-wave ultraviolet light (UV). Twenty-four such mutants were studied. They all show Mendelian segregation in crosses with wild type. Plasmodia constructed from mutant amoebae were all deficient in deoxythymidine incorporation. Extracts made from selected plasmodia showed that all except one had low thymidine kinase activity.

Genetical and biochemical complementation studies revealed two complementation groups: 23 mutants, bur A, had low thymidine kinase while 1 mutant, bur B, had normal thymidine kinase levels.

Growth of E. coli K12 in the presence of chlorpromazine or promethazine resulted in the appearance of a special kind of mutational change with a frequency of 5–10%. These cells were UV-sensitive and very mucoid in their colony formation. The strains were characterized as colanic acid producing on the basis of phage m-59 sensitivity and we tentatively conclude that these mutants are Lon−.

In another series of experiments drug treatment of E. coli failed to yield significant numbers of auxotrophs and the back mutation rate of a number of S. typhimurium His− strains was not significantly increased.

Thymineless strains of Escherichia coli C600 were constructred harbouring both an R factor of the N incompatibility group (R46 or R447b) and a compatible plasmid (Plac- of the A-C group or the Iα plasmid R62), which contained a segment of N group DNA. Selection was made for the transferred plasmid and dislodgement phenomena were manifest either as loss of an entire plasmid or as deletions of a region of plasmid DNA. Even after the two R factors had become established as separate replicons, the N group R factor but not the other plasmid exhibited instability.

Thymine starvation of strain C600 thy (R447b/R62) increased the elimination rate of the N group plasmid R447b but no elimination of R62 was observed. However, thymine starvation of strain C600 thy (R46/Plac-) not only increased the rate of elimination of R46 but also increased the rate of loss of Plac-. There was no detectable increase in nuclease activity in unstarved R46/Plac- strains and it is concluded that dislodgement of R46 from these strains is not due to induction of the nuclease that has been proposed to be responsible for the elimination of N group plasmids during thymine starvation.

Two variants of Plac- were isolated. These did not dislodge R46 from unstarved R46/Plac- strains and were not lost during thymine starvation even though thymineless elimination of R46 occurred at normal frequency.

The gene pfpr-10 in Coprinus confers resistance to p-fluorophenylalanine. The resistance of the heterozygote pfpr-10/pfp8-10 is completely recessive, both in diploids and dikaryons. A dominance modifier Mod+ makes pfpr-10 dominant in a dikaryon but not in a cliploid. It also enhances the degree of resistance in r homozygotes. These results are explained on a hypothetical model based upon a hexameric product of the pfpr-10 gene, with resistance to PFP being proportional to the percentage of homo r hexamers. The Mod+ is presumed to act by keeping the r and s products separate so that hybrid multimers are reduced to a minimum. Critical threshold concentrations of PFP for diploid/haploid dikaryons in 40 different combinations of pfpr and Mod+ genes cover a wide range of gene doses and percentage of homo r multimers. The relationship between the critical threshold concentrations and the calculated percentage of homo r multimers supports the model.

Thirty-nine enzyme loci and seven non-enzymic protein loci have been screened for electrophoretically detectable variation in a population of Pleuronectes platessa, a marine flatfish. The mean heterozygosity per individual is 0·102 ± 0·026, or 0·118 ± 0·030 if the non-enzymic proteins are excluded. The distributions of allele frequencies and single locus heterozygosities are given, and the results discussed with reference to current theories concerning the nature of protein variation.

The genetic properties of some new mutant t-haplotypes derived from the naturally occurring haplotype t6 have been investigated. Several mutant haplotypes gave taillessness with brachyury, T, were viable when homozygous, and when in compound with t6, and all these expressed tf and appeared to have arisen by meiotic crossing-over between T and tf in the region of crossover-suppression of t6. The haplotype th17 arose by crossing-over in a stock of t6 carrying the translocation T(1; 17) 190Ca, in which the translocation break in chromosome 17 is within the crossover-suppressing region; hence th17 could not be separated from T190. It was of the complementary crossover type in that it did not interact with T, and was lethal in compound with t6; its male segregation ratio was normal with heterogeneity. A further haplotype, th20, expressed tf, gave taillessness with T, and was lethal when homozygous and in compound with t6. The expression of tf was attributed to a deletion, which also covered the loci of the nearby lethals knobbly, Kb, and tw5. th20 showed weak complementation of tw5. The haplotype th7 had previously been interpreted as carrying a duplication; it was shown that this duplication was semi-lethal when homozygous. it is suggested that lethal mutant t-haplotypes commonly arise by duplication or deletion but such structural changes are not necessarily at the end of the haplotype, and need not arise by unequal meiotic crossing-over.

Large reciprocal differences in recombination frequencies were observed in F1 female progeny of a number of strain crosses. These reciprocal effects on recombination were found in several intervals of all three major chromosomes; they were greatest in intervals proximal to or spanning the centromere but were also found in some distal regions. The direction of recombination change was not consistent over different chromosomal intervals. There was no clear trend for reciprocal recombination differences to be associated with change of interference values between adjacent intervals. A close association was found between reciprocal female recombination effects, male recombination and other component traits of hybrid dysgenesis. However, reciprocal differences in female recombination were not restricted to dysgenic crosses. Backcross experiments demonstrated that reciprocal differences in the centromeric region of chromosome III were the result of increased crossing-over in dysgenic F1 hybrids rather than decreased crossing-over in the reciprocal hybrids. It is concluded that genotype-cytoplasm interaction can be a major factor influencing recombination frequencies and that the use of interstrain hybrids for recombination measurement may lead to errors in the estimation of intrastrain frequencies.

The gene conversion model reported by Birky & Skavaril (1976) has been analytically studied by using the theory of diffusion models of Kimura (1964) in population genetics. It has been shown that the fate of new mutations in systems with multiple genomes may be satisfactorily treated by the diffusion model.