It is hypothesized that the products of Neurospora rec+ genes mask recombinators such as cog by modifying DNA and that unmodified recombinators act as recognition sites for an endonuclease with scission properties like those of the type I restriction enzymes found in E. coli. These cut the DNA in both strands at some variable distance from a recognition site. Repair of a two strand gap initiated in this way would require DNA synthesis using the information contained in the homologous DNA duplex, leading to gene conversion. Crossing over could follow from resolution of two Holliday structures formed during gap repair. The hypothesis explains the polarity in the frequency of conversion events across genetic loci, the observation that chromosomes carrying recombinators are more often converted than is the homologue, and how recombinators can initiate conversion at a distance, as suggested by the pattern of conversion events in the his-3 locus in crosses heterozygous for the translocation TM429.

In eukaryotic chromosomes, large blocks of satellite DNA are associated with regions of reduced meiotic recombination. No function of highly repeated, tandemly arranged DNA sequences has been identified so far at the cellular level, though the structural properties of satellite DNA are relatively well known. In studying the joint action of meiotic recombination, genetic drift and natural selection on the copy number of a family of highly repeated DNA (HRDNA), this paper looks at the structure–function debate for satellite DNA from the standpoint of molecular population genetics. It is shown that (i) HRDNA accumulates most probably in regions of near zero crossing over (heterochromatin), and that (ii), due to random genetic drift the effect of unequal crossover on copy numbers is stronger, the smaller the population size. As a consequence, highly repeated sequences are likely to persist longest (over evolutionary times) in small populations. The results are based on a fairly general class of models of unequal crossing over and natural selection which have been treated both analytically and by computer simulation.

Over one hundred backcross-one progeny were analysed by two dimensional electrophoresis to locate the genes on the short arm of chromosome 1D which code for, or control, the D group of LMW glutenin subunits. Recombination between these genes and Glu-D 1, encoding HMW glutenin subunits, was frequent but none could be detected between the D subunit genes and Gli-D1, coding for ω-gliadins, γ-gliadins and the B group of LMW glutenin subunits. These results are in contrast to those for chromosome 1 B because apparently homoeologous D subunit genes occur at a different position, being equidistant between Glu-B 1 (homoeologous to Glu-D 1) and Gli-B 1 (homoeologous to Gli-D 1). A range of 18 genetically-diverse wheat varieties, each containing one of two allelic groups of 1 D-encoded D subunits, were also analysed by two-dimensional electrophoresis. Consistent with the genetic analysis above, unbreakable linkages were found between these alleles and alleles of Gli-D 1. The results are discussed in relation to the evolution of the distribution of prolamin genes in the wheat genome.

Several strains have been synthesized which have reactive (R) properties in the I–R system of hybrid dysgenesis and which are also classified as active P strains in the P–M system. The synthesis of this previously unknown combination of types was accomplished by employing a mating scheme which allowed transposition (chromosomal contamination) of P, but not I, factors from IP to RM chromosomes in dysgenic F1 males. The successful synthesis of RP strains provides strong evidence that the apparent absence of this combination in natural and laboratory populations of melanogaster is not due to a biological incompatibility between these two types.

N-ethyl-N-nitrosourea (ENU) was used to induce mutations within the tw5-haplotype of the mouse to make possible a further study of gene arrangement in t-mutants and to provide potential landmarks for cloning and sequence studies in the region. Two independent mutants were isolated for each of three loci in the t-region, brachyury (T), quaking (qk), and tufted (tf). The new Tkt alleles produce tailless mice when a tct mutation is present in trans. The new qkkt alleles are recessive and homozygous lethal. They are viable, male fertile, and cause seizures and quaking when paired with the qk mutation which previously defined the locus. The tfkt mutations are recessive and phenotypically similar to the mutant alleles available in non-t chromosomes. The mutations were induced in the tw5-haplotype at an average per locus frequency of 1 in 1500. Their isolation demonstrates the power of this technique for obtaining the specific mouse mutants that are needed to genetically dissect a complex mammalian system.

Isoelectrofocusing two-dimensional polyacrylamide gel electrophoresis (IEF-2D-PAGE) offers the opportunity to detect typical alterations in the protein pattern of trisomic mouse foetuses at a given time of development. The fractionation of the cell lysate by differential centrifugation into various subcellular components (nuclei, membranes, polyribosomes, cytoplasmic proteins) and fractionation of the proteins through DEAE-Sepharose chromatography allows detection of protein differences.

It is possible to detect eight differences in the protein patterns between trisomy 19 (Ts 19) mouse foetuses and euploid mouse fetuses at day 15. Five of these differences are quantitative in nature, three are qualitative. One of these proteins is synthesized in Ts 19 foetuses at a higher level than in euploid mouse fetuses (primary gene dosage effect). The other seven proteins are reduced or not present in trisomic foetuses (consequences of primary gene dosage effects).

The molecular mass of the individual proteins ranges from 13 to 41 kDa.

5-azacytidine-treated human fibroblasts exhibit a significant decrease in the frequencies of Barr body+ cells as compared to nontreated cultures. This presumably indicates that 5-azacytidine can induce a change in the degree of condensation of the Barr body. It is suggested that the state of chromatin condensation of the Barr body may be related to the reactivation process by 5-azacytidine of gene loci in the inactive X.

Mating competition experiments with D. melanogaster were performed in light and darkness under conditions mimicking those under which artificial populations show a stable polymorphism for the ebony gene (e). In both light and darkness a minority male mating advantage was found for e/ + males in competition with wild-type males, but in light only when ebony was in the majority. Homozygous wild-type males showed minority advantage only in light and ebony males only in darkness.

The maintenance of polygenic variation through a balance between mutation and stabilizing selection can be approximated in two ways. In the ‘Gaussian’ approximation, a normal distribution of allelic effects is assumed at each locus. In the ‘House of Cards’ approximation, the effect of new mutations is assumed to be large compared with the spread of the existing distribution. These approximations were developed to describe models where alleles may have a continuous range of effects. However, previous analyses of models with only two alleles have predicted an equilibrium variance equal to that given by the ‘House of Cards’ approximation. These analyses of biallelic models have assumed that, at equilibrium, the population mean is at the optimum. Here, it is shown that many stable equilibria may coexist, each giving a slight deviation from the optimum. Though the variance is given by the ‘House of Cards’ approximation when the mean is at the optimum, it increases towards a value of the same order as that given by the ‘Gaussian’ approximation when the mean deviates from the optimum. Thus, the equilibrium variance cannot be predicted by any simple model, but depends on the previous history of the population.