The nucleotide sequence data from highly repeated DNAs of inverte-brates and mammals are summarized and briefly discussed. Very similar conclusions can be drawn from the two data bases. Sequence complexities can vary from 2 bp to at least 359 bp in invertebrates and from 3 bp to at least 2350 bp in mammals. The larger sequences may or may not exhibit a substructure. Significant sequence variation occurs for any given repeated array within a species, but the sources of this heterogeneity have not been systematically partitioned. The types of alterations in a basic repeating unit can involve base changes as well as deletions or additions which can vary from 1 bp to at least 98 bp in length. These changes indicate that sequence per se is unlikely to be under significant biological constraints and may sensibly be examined by analogy to Kimura's neutral theory for allelic variation. It is not possible with the present evidence to discriminate between the roles of neutral and selective mechanisms in the evolution of highly repeated DNA.

Tandemly repeated arrays are constantly subjected to cycles of amplification and deletion by mechanisms for which the available data stem largely from ribosomal genes. It is a matter of conjecture whether the solutions to the mechanistic puzzles involved in amplification or rapid redeployment of satellite sequences throughout a genome will necessarily give any insight into biological functions.

The lack of significant somatic effects when the satellite DNA content of a genome is significantly perturbed indicates that the hunt for specific functions at the cellular level is unlikely to prove profitable.

The presence or in some cases the amount of satellite DNA on a chromosome, however, can have significant effects in the germ line. There the data show that localized condensed chromatin, rich in satellite DNA, can have the effect of rendering adjacent euchromatic regions rec−, or of altering levels of recombination on different chromosomes. No data stemming from natural populations however are yet available to tell us if these effects are of adaptive or evolutionary significance.

We have examined the major urinary protein (MUP) phenotype of three inbred mouse strains by one-dimensional isoelectric focusing in acrylamide gels. Each strain gave a distinct pattern of major and minor bands. In the three strains together, seven major and about seven minor bands were observed. F1 phenotypes were intermediate. F2 phenotypes can be explained by recombination between allelic variants at four or more different genetic loci. We propose that variation in MUP phenotype is due in fact, to allelic variation at approximately seven structural gene loci, some of which are linked on chromosome 4. The remainder may or may not be linked to these.

Seven third chromosome samples from laboratory populations and one from a wild population were classified by their genotypes at five allozyme loci and by the occurrence of lethals. The data were analysed for independence among classifications by a randomization method, and it was found that when the number of classifications is high the independence hypothesis does not hold. We have split the independence hypothesis among populations and have found that the lack of fit to the hypothesis comes mainly from the wild population. As one of our classifications was lethality, these findings seriously question the interpretation of multilocus fitness estimations. To split the independence hypothesis into interactions, the criterion of Bartlett for non-interaction with exact probability methods was used; interactions at the levels of pairs and triplets were not significant as a whole. It was not possible to carry the interaction analysis any further as the frequencies of chromosomal types were completely determined by their marginal totals at orders of interaction higher than that of triplets. Available parametric estimations of these high order interactions are therefore of dubious meaning. The analyses of chromosome samples and the temporal surveys of population cages described here, as well as data from the literature, suggest that the Est 6-Pgm region is prone to show disequilibrium.

A general model of linked genes or a part of a genome is proposed which enables us to study various problems in molecular population genetics in a unified way. Several formulae with special reference to the linkage disequilibrium and genetic distance are derived for neutral mutations in finite populations, based on the method of diffusion equations. It is argued that the model and formulae are useful particularly when observations are made in terms of DNA sequence.

The various lethal t-haplotypes are divided into several complementation groups defined by lethality of tx/ty heterozygotes, and only partial complementation is usually observed in heterozygotes between t complementation groups. Several effects of the t region have been found to be preferentially or exclusively detectable in males. This paper describes results showing that the viability of t6/tw5 heterozygotes is influenced by the sex of the embryo; female viability is only slightly reduced (viability ratio approximately 0·80), while male viability is far below normal (0·25).

A diploid heteroallelic at the gal1 locus and producing little residual galactokinase activity was chosen. Following either γ- or UV-irradiation, recombination occurred leading to the formation of wild-type GAL1 genes and an increase in detectable galactokinase. An enhanced level of enzyme was first detectable 2 h after irradiation and reached a maximum within 12–14 h. With increasing doses of irradiation, more enzyme was produced and this increase superficially resembled that obtained for plated recombinants. However, far more enzyme was actually synthesized than expected from the number of viable recombinants in the cells assayed. This suggests that recombination must have occurred in cells without colony-forming ability, indeed it may have occurred more frequently in these cells than in viable cells.

Monosomic and disomic substitutions of Imperial rye chromosome C for 4A of Chinese Spring wheat were analysed for two enzyme markers, alcohol dehydrogenase (ADH) and 6-phosphogluconate dehydrogenase (6-PGD). The gene(s) coding for ADH and 6-PGD were located on the short and long arms of rye chromosome C respectively.

Isozyme analyses revealed that the substitute chromosome was a translocation involving alpha arm of wheat chromosome 4A and long arm of rye chromosome C. Pairing behaviour of the substitute chromosome with rye and wheat chromosomes in hybrids with rye addition line C and ditelosomic 4A (alpha) confirmed this.