The insertion of a high-copy-number plasmid into a lambdoid phage chromosome which lacks a functional repressor gene confers on the hybrid ‘phasmid’ the capacity to grow on an immune lysogen. This was found to be due to titration of repressor because of plasmid replication. We have exploited this property in order to isolate mutants that affect plasmid replication. These mutants have been mapped in a region that was previously characterized as necessary for plasmid replication and incompatibility properties. Some of the mutations could revert at frequencies characteristic of single-base-pair change mutations.

The results of the analysis of 393 mitotic recombinants within the paba1 region of Aspergillus nidulans can be summarized as follows:

1. Reciprocal, non-reciprocal and probably inexactly reciprocal exchanges occur in intra-cistron mitotic recombination.

2. Negative interference observed in intra-cistron mitotic recombination in the paba1 region of Aspergillus nidulans is more intense than that observed in meiotic recombination in the same cistron.

3. In intragenic mitotic recombination multiple exchanges can involve three or even four chromatids within one effective pairing segment.

A cryptic, lethal t haplotype (named tLmb) has been discovered in the non-inbred MF1 laboratory stock of mice. Detailed genetic and molecular studies demonstrate a close relationship between tLmb and a well-studied t haplotype, t6, previously extracted also from a laboratory stock. It appears likely that t6 is an aberrant t haplotype derived by recombination from a tLmb-like ancestral chromosome. The persistence of tLmb through 40 years of random breeding in a laboratory stock indicates that high transmission ratio distortion is sufficient to overcome the deleterious effect of a recessive lethal gene in a mouse population.

Cold-resistant revertants of the cold-sensitive, ribosomal suppressor suaC109 have been isolated, with a view to obtaining mutations in new ribosomal protein genes. Many revertants had reduced suppressor activity and were classified as antisuppressor mutants. Both intragenic and extragenic reversions were found. In seven strains the extragenic reversion to cold resistance segregated with the antisuppressor phenotype, and these were designated asu mutations. Three of the five asu genes, C, B and D were mapped to linkage groups, I, II and V respectively. The antisuppressors are not gene-specific, although they mainly antagonize the activity of ribosomal suppressors. The antisuppressors altered all aspects of the phenotype of suppressor suaC109 including sensitivity to aminoglycoside antibiotics, and are therefore thought to be mutations in ribosomal protein genes.

The extent and phenotype of acriflavin-resistant rII deletions have been examined. The properties of these deletions confirm that acriflavin resistance may result from a loss of function at the ac locus and that the ac locus coincides with the rII distal portion of the dispensable region which is adjacent to the rIIB cistron.

The frequency of the more common patterns of non-disjunction in Neurospora was studied. Detection of these asci was accomplished by the use of pantothenate requiring strains grown on reduced amounts of pantothenate, so that combinations of dark, pale, and aborted spores provided evidence of non-disjunction. The isolates from five non-disjunction asci were examined in detail and an apparently high frequency of mitotic recombination was detected for presumed disomic isolates. An hypothesis concerning a mechanism of non-disjunction is presented.

The age of an allele segregating in a finite population may be defined in two ways. They are (1) the age of a mutant gene that has never reached fixation in the population, and (2) the age including any fixation period in the past. Theoretical expressions for these are derived on the assumption that every mutant is unique.

Detailed physiological and genetic studies of haploid and diploid strains have revealed a complex phenotype for the rec-1 mutation in Ustilago maydis. The mutant is defective in the repair of damage by UV light, ionizing radiation and nitrosoguanidine. Four alleles are all recessive and have the same sensitivity to UV, suggesting the loss of a single cellular function. A significant fraction of non-viable cells is formed during growth, and in diploid strains considerable variation in colony size and morphology is seen. The spontaneous frequency of mutation is greater than in wild-type cells, but there is little, if any, enhancement by irradiation.

rec-1 also has pleiotropic effects on genetic recombination. The spontaneous level of mitotic allelic or non-allelic recombination is abnormally high, but the relative increase after irradiation is much lower than in control diploids. Allelic recombination is strongly associated with the expression of a hetozygous recessive distal marker, and it is shown that this is often due to hemizygosity rather than to homozygosity of this marker. The results indicate that allelic recombination is due to crossing over rather than gene conversion, but that the cross over is often associated with a chromatid break. rec-1 interacts with other radiation sensitive mutants, such as rec-2. Diploids homozygous for both are totally deficient in allelic recombination. In crosses between rec-1 strains meiosis is defective, with a low viability of meiotic products and frequent production of aneuploids or diploids among the survivors. The overall phenotype of rec-1 strains can best be explained in terms of the loss of a regulatory function, which leads to uncontrolled recombination during mitosis and meiosis, and the loss of a recombination repair pathway which is normally induced by agents which damage DNA.

This paper studies the influence of two opposite forces, unidirectional unconditionally deleterious mutations and directional selection against them, on an amphimictic population. Mutant alleles are assumed to be equally deleterious and rare, so that homozygous mutations can be ignored. Thus, a genotype is completely described by its value with respect to a quantitative trait x, the number of mutations it carries, while a population is described by its distribution p(x) with mean M[p] and variance V[p] = σ2[p]. When mutations are only slightly deleterious, so that M » 1, before selection p(x) is close to Gaussian with any mode of selection. I assume that selection is soft in the sense that the fitness of a genotype depends on the difference between its value of x and M, in units of σ. This leads to a simple system of equations connecting the values of M and V in successive generations. This system has a unique and stable equilibrium, where U is the genomic deleterious mutation rate, δ is the selection differential for x in units of σ, and p is the ratio of variances of p(x) after and before selection. Both δ and ρ are parameters of the mode of soft selection, and do not depend on M or V. In an equilibrium population, the selection coefficient against a mutant allele is ŝ = δ2[U(2–ρ)]−1. The mutation load can be tolerable only if the genome degradation rate υ = U/σ is below 2. Other features of mutation-selection equilibrium are also discussed.

This paper tests the hypothesis that haplodiploidy or X linkage leads to less genetic variability. Although haplodiploid organisms exhibit a low level of genetic variability the wide variation existing between different diploid organisms implies that factors other than the genetical system could also be responsible. In order to test the hypothesis critically it is necessary to compare the level of genetic variability between X-linked and autosomal genes within a closely related group of organisms. For kangaroos, the ascertainment bias for X-linked loci has been removed by assuming the correctness of Ohno's law of conservation of the mammalian X, i.e. that genes found to be X-linked in man can be assumed to be X-linked in kangaroos. For Man and Drosophila, it has been assumed that the percentage of the karyotype which is X chromosome can be used as the expectation for the percentage of X-linked polymorphisms. No difference between the two classes of loci is evident in kangaroos and man for percentage polymorphism. The data however have confidence limits which would allow autosomal loci to have three times greater percentage polymorphism. In Drosophila the published data of Prakash show that autosomal loci are polymorphic about twice as frequently as are their X-linked counterparts. Thus there may be a modest reduction in percentage polymorphism as a result of X-linkage (i.e. haplodiploidy). No reduction in the number of alleles per locus or average heterozygosity at those loci which are polymorphic is evident in kangaroos, man, or Drosophila. More data on more X-linked enzymes are necessary to establish firmly that there is a real reduction in percentage polymorphism and to estimate its extent. The kangaroo data are incompatible with the hypothesis that a large fraction of the variability is maintained by simple overdominance since overdominance is very unlikely in the quasi-haploid genetical system which results from the paternal X inactivation mode of dosage compensation used by kangaroos. This is the first report on level of enzymic variability in marsupials. 17% of autosomal loci and 18% of X-linked loci are polymorphic, average heterozygosity is 4% for autosomal and 4% for X-linked loci and number of alleles per locus is 1·25 for autosomal and 1·21 for X-linked loci. These figures are somewhat lower than for eutherian mammals.

Pod shattering of rapeseed (Brassica napus) causes serious yield loss. Genetic resistance to shattering has been introgressed into B. napus from B. juncea. This followed from allosyndetic pairing between chromosomes of B and C genomes in the interspecific F1 hybrid, B. juncea × B. napus (2n = 37, AABC). The reconstituted B. napus plant showed regular meiosis with 19 bivalents and had pollen and seed fertility of 84 and 23% respectively. An approach is suggested for achieving introgression from monogenomic diploids to digenomic allopolyploids that exploits non-homologous recombination.

Genetic variation in the modulating effect of dietary sucrose was assessed in Drosophila melanogaster by examining 27 chromosome substitution lines coisogenic for the X and second chromosomes and possessing different third isogenic chromosomes derived from natural populations. An increase in the concentration of sucrose from 0·1% to 5% in modified Sang's medium C significantly altered the activities of 11 of 15 enzyme activities in third instar larvae, indicating that dietary sucrose modulates many, but not all, of the enzymes of D. melanogaster. A high sucrose diet promoted high activities of enzymes associated with lipid and glycogen synthesis and low activities of enzymes of the glycolytic and Krebs cycle pathways, reflecting the physiological requirements of the animal. Analyses of variance revealed significant genetic variation in the degrees to which sucrose modulated several enzyme activities. Analysis of correlations revealed some relationships between enzymes in the genetic effects on the modulation process. These observations suggest that adaptive evolutionary change may depend in part on the selection of enzyme activity modifiers that are distributed throughout the genome.