A barley endosperm cDNA clone was used to study the polymorphism and chromosomal location of β-amylase genes in barley. Analysis of DNA from seven cultivars digested with three restriction endonucleases showed two types of pattern, one present in Sultan and the other in the remaining six cultivars. A copy-number reconstruction indicated the presence of about three gene copies per haploid genome. Analysis of the six available whole chromosome addition lines and selected telocentric chromosome additions of barley into wheat showed the location of genes on the short arm of chromosome 2 (probably one copy) and the long arm of chromosome 4 (probably two copies).

By analogy with the situation in coccids it is suggested that in mammalian XO embryos the single X turns heterochromatic in some cells, but that such a change does not result in cell death because the X then reverts back to an euchromatic and active state. This testable alternative to the Gartler–Sparkes hypothesis would imply that the anomalies of the XO Turner syndrome are largely due to imbalance of sex-linked genes rather than developmental damage resulting from cell death and that mammalian X inactivation might become reversed in response to special developmental needs.

1. Four lines selected for large size were crossed to form a base population for further selection for high 6-week weight; three small lines were crossed similarly, and the crossbred population was selected for low 6-week weight.

2. In every case, a cross between two selected lines resulted in heterosis increasing body weight. This shows that all of the selected lines were differentiated with respect to genes affecting body weight.

3. Further selection for large size produced a stock whose mean weight was 25% higher than the largest of the original lines at its limit. But the response to selection for small size was slow, and after twenty-four generations of selection, the low weights of two of the original lines had not been recovered.

4. The evidence points to linkage of genes affecting body weight in the mouse. It is suggested that this is a particular feature of crosses between previously selected lines, rather than a general feature of mouse populations.

Almost nothing is known about the identity of the genes causing reproductive isolation between species. As a first step towards molecular isolation of a ‘speciation gene’, I mapped and partly characterized a gene causing hybrid male sterility in Drosophila. This analysis shows that sterility of D. melanogaster males who carry the ‘dot’ fourth chromosome from D. simulans is due entirely to a very small region of the D. simulans chromosome (including only about 5 salivary gland bands or approximately 250 kb of DNA). Thus the hybrid sterility effect of the D. simulans fourth chromosome is almost surely due to a single gene of very large effect (here named hms, hybrid male sterile). Hms is zygotically acting, and the D. simulans allele of hms is completely recessive. Furthermore, complementation tests suggest that hms is not an allele of any known locus in D. melanogaster.

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.

The Neurospora crassa photoreactivating enzyme has been assayed for by the Hemophilus influenzae and Bacillus subtilis transformation systems. In contrast to the H. influenzae system, u.v.-treated transforming DNA from B. subtilis did not give evidence of reactivation of u.v. lesions by crude enzyme extracts from N. crassa when exposed to photoreactivating light. The u.v. dose required to inactivate B. subtilis transforming DNA is about ten times that required to inactivate H. influenzae DNA to the same level of survival. This difference in dose required to inactivate DNA's of about the same base composition probably reflects the greater u.v. resistance of the B. subtilis recipient strains used. Hypotheses are considered which suggest that N. crassa crude enzyme extracts contain either nucleases which degrade B. subtilis transforming DNA excessively or an inhibitory factor which affects the transformation process itself.

Selection for increased and for decreased expression of the sex-linked gene brindled (Mobr) in heterozygous females produced two lines with non-random X chromosome inactivation. In the High line the X chromosome marked by brindled was active in about 60% of cells, while in the Low line it was active in about 25% of cells. The whole of the difference was caused by the chromosomes carrying brindled: neither the unmarked X chromosome nor the autosomes were differentiated. There was a positive correlation between the expression of brindled in daughters and mothers. This was probably not caused by residual genetic variation, but was more probably a maternal effect similar to that described by Cattanach & Papworth (1981). On this assumption the daughters' scores were adjusted to a standard maternal score. Enzyme assays on females doubly heterozygous for brindled and for the sex-linked Pgk-1 locus proved that the percentage of brindled in the coat provided an accurate measure of the X-inactivation proportions in the blood, liver and kidney. The accuracy was improved by adjustment for maternal score. In the selection lines, brindled was always inherited from the mother. When brindled was transmitted by male parents the probability of activation of its chromosome was increased by 8 percentage points in the High line and 18 in the Low line. This effect of the parental source is much greater than has previously been reported. The responses to selection can be interpreted in terms of the Xce locus controlling the activation probability, different alleles on the chromosomes carrying brindled being selected in the two lines. If this interpretation is correct, the alleles on one or both of the chromosomes carrying brindled were different from any of the three known alleles. The different effects of male transmission in the two lines can be described as a difference between the two chromosomes in their reactions to imprinting. This difference might possibly also be due to the Xce locus.

The competitive-index method of measurement of over all fitness in Drosophila has been used to measure the effect of inbreeding and of artificial selection for metric characters in a large population of Drosophila melanogaster. The technique itself was examined in detail with particular reference to its repeatability and to the effect on it of the modification of various environmental variables.

With continued full-sib mating the decline in the competitive index was very rapid (it was reduced to a half by a single generation of full-sib mating) and there were no indications that interactions between deleterious genes at different loci were important in determining the rate of decline of fitness as inbreeding increased. Other unselected lines with ten pairs of parents in each generation were carried to serve as a control for the lines under artificial selection. At the same theoretical degree of inbreeding the control lines had a much higher average fitness than the lines produced by continued full-sib mating.

From the base population lines were selected in both directions for abdominal bristles, sternopleural bristles and for wing length, there being two replicates in all cases. Four control lines were kept with the same number of parents as the selected lines. In all cases the selected lines declined in fitness below the value for the base population. However, in three of the lines the fitness was not significantly below the value for the control lines. The effect of artificial selection on fitness was asymmetrical, the decline being greater with down selection for all characters.

The relevance of these results to various theoretical models is discussed. If the variation in these characters is actively maintained in the base population by the selection of heterozygotes then the results are consistent with an average selection disadvantage of homozygotes relative to heterozygotes of about 0·5%.

Four isolated populations of the skipper frog, Rana cyanophlictis were first studied in 1965 and then again in 1975. The genetical changes were measured by the incidence of 19 non-metrical skeletal variants. It was found that these populations have changed very little in 10 years, although the inter-population diversity, as judged by the estimates of divergence, is less now than previously. This could be due to the similar environmental conditions prevailing in Delhi and its neighbourhood from where these frog populations were collected.

I factors are transposable elements of Drosophila melanogaster similar to mammalian LINEs, that transpose by reverse transcription of an RNA intermediate and are responsible for the I–R system of hybrid dysgenesis. There are two categories of strains in this species: inducer, that contain about 15 I elements at the various sites on chromosomal arms, and reactive, that lack active I factors. I elements occur in various Drosophila species. Potentially functional I factors from Drosophila teissieri can transpose when introduced by P-element-mediated transformation in a reactive strain of Drosophila melanogaster. We have studied the properties of Drosophila melanogaster strains into which such an I factor from Drosophila teissieri, named Itei, was introduced. Typical hybrid dysgenesis is produced when males carrying Itei are crossed with reactive females. However, more than one copy of the element seems necessary to produce dysgenic traits, whereas only one I factor of Drosophila melanogaster seems to be sufficient. The copy number of Itei in transformed lines maintained by endogamous crosses increases rapidly and stabilizes at values similar to those observed in inducer strains. As Drosophila teissieri contains much fewer copies than the Drosophila melanogaster strains, this suggests that the copy number of I elements is not simply regulated by sequences present in the element itself.