rpoB is the structural gene for the β-subunit of E. coli RNA polymerase. The rpoB-3 allele confers resistance to the antibiotic rifampicin and is unusual in being dominant to the wild-type allele. We used the plasmid pZD23, a derivative of the broad host range conjugative plasmid RP4, to introduce the rpoB-3 allele into a range of bacterial species. Species belonging to the same family as E. coli (Enterobacter aerogenes, Citrobacter freundii, Hafnia alvei møller, Klebsiella pneumoniae, Salmonella typhimurium) expressed rpoB-3 to give a rifampicin resistant phenotype; this demonstrated heterospecific transcription. The transfer of pZD23 to the non-Enterobacteriaceae species Azotobacter vinelandii and Rhizobium leguminosarum did not result in rifampicin resistance. In the former case this was due to non-expression of the rpoB-3 resistance phenotype, in the latter case the dominant resistance phenotype had been lost from pZD23. Heterospecific transcription can be used as a criterion for the investigation of genetic relatedness between bacterial species.

Six wheat/Agropyron intermedium addition lines are described on the basis of their phenotype and biochemical markers. An assessment of homoeology of each addition chromosome is made. Chromosome morphology, plant phenotype, isozyme and protein studies are compared with similar data for other wheat/alien addition lines and other members of the Triticeae. These comparisons give consistent results and it is concluded that addition lines L1, L2, L3, L4, L5 and L7 carry Agropyron chromosomes of homoeologous groups 7, 3, 1, 4, 5 and 6 respectively. This agrees with previously published work with one exception: the L5 chromosome belongs to homoeologous group 5 and not group 2 as proposed by Figueiras et al. (1986).

The P–M system of hybrid dysgenesis in Drosophila melanogaster is a syndrome of genetic abnormalities which appears in the progeny of crosses between strains different with regard to their possession of ‘P’ transposable elements. Cytotype is an extrachromosomal property which regulates the mobility of the P element. We report here data showing that a cytotype polymorphism previously observed in a natural population from North-Africa is stable over a period of 5 years. A potentially high rate of mutation is associated with this cytotype polymorphism. Explanations of the appearance of a cytotype polymorphism are proposed and the consequences for the genetic load induced by transposable elements are discussed.

Many inbred and isofemale lines derived from wild populations of Drosophila melanogaster were tested for gonadal dysgenic sterility, male recombination and snw secondary mutation. Among them, we have found strains whose dysgenic offspring show negligible sterility, and undetectable male recombination and snw mutation. They can be considered to be neutral strains in the strict sense. Such neutral strains appear to carry only defective P elements in their genomes. Taking the observations of Karess & Rubin (1984) into account, it is suggested that some defective P elements retain the function necessary for P cytotype. Cytotype determination mechanisms are discussed.

Sex determination in Drosophila depends on the ratio of X chromosomes to sets of autosomes (X:A). This chromosomal signal is used to regulate a few control genes whose state of activity selects either the male or the female sexual pathway. We have studied the structure and function of dsx (double sex) which appears to be the last regulatory gene on whose function the sexual pathway eventually depends. We have mutagenized the locus, varied the doses of dominant dsx-mutations and wildtype alleles, and combined different dsx-alleles with recessive mutations in other sex-determining genes, such as ix, tra-2 and tra.

The locus dsx harbours two genetic functions, dsxm to implement the male program, dsxf to implement the female program. We found that dsxm and dsxf can mutate independently although most mutations abolish both functions. We conclude that dsxm and dsxf each have their specific domain, but also share a large region of DNA that is essential for both functions. We present evidence that the dominant mutations correspond to a constitutive expression of the male-determining function dsxm, with the simultaneous abolishment of the female-determining function dsxf. This effect can be counteracted by two doses of expressed dsxf so that a female phenotype results. The products of one dose of expressed dsxm and one dose of expressed dsxf in the same cell appear to neutralize each other which leads to a null phenotype. The mutant combinations suggest that the product of dsxf requires the products of ix+, tra-2+ and tra+ to become functional.

In Lucilia cuprina (Wiedemann) females, non-segregation of compound fifth-chromosomes is correlated with non-disjunction of the X chromosomes. Approximately two-thirds of eggs which inherit both maternal compound elements are nullo-X, suggesting that meiotic pairing between X chromosomes and compound autosomes has occurred. There was no evidence for pairing of the compounds and the X or Y chromosome in males. A limited amount of data suggests that high non-segregation frequencies may occur in the offspring of putative X/X/X and X/O females. These results suggest the existence of non-homologous (distributive) pairing in L. cuprina females.

The OTC gene coding for ornithine transcarbamylase is sex linked and subject to X inactivation in humans and mice. We have used a rat cDNA probe to localize OTC by in situ hybridization in marsupials and monotremes. The gene maps to an autosomal site in two distantly related marsupial species and in one monotreme (the platypus); the first demonstration that a gene X-linked in one mammalian species may be autosomal in another. Since the conservation of the mammalian X is thought to be a consequence of its isolation by the inactivation mechanism, we propose that an autosomal or pseudoautosomal segment containing OTC has been recruited into the inactivated region of the X rather recently in eutherian evolution while it remained autosomal, or was translocated to an autosome, in metatherian and prototherian mammals.

Five class II H-2 genes borne by t chromosomes were partially sequenced: borne by the tTuw10 chromosome of EDY589 (H-2w2); and borne by the tTuw8 chromosome of CR0437 (H-2w57), as well as and borne by the tTuw7 chromosome of CR0435 (H-2w37). These genes are representatives of the three major groups of alleles found associated with t chromosomes. The sequenced part consisted of almost the entire exon 2 and the entire exon 3 coding for the first and the second domain of the β polypeptide chains, respectively. The sequence was compared with the published sequences of Aβ and Eβ alleles borne, by non-t chromosomes. The comparison revealed that the t-associated alleles are no more similar to one another than they are to the corresponding genes present on non-t chromosomes in laboratory mice. This divergence in the nucleotide sequence among the class II genes is interpreted as evidence that the t complex is very old.

In the mouse histidinaemia has a teratogenic effect. Animals subjected to high levels of histidine in utero may develop inner ear and behavioural abnormalities typical of the ‘shaker–waltzer’ syndrome. Selection procedures for abnormalities and relaxation of selection have resulted in two histidinaemic strains: the Cambridge strain in which abnormalities occur in over 80% of animals, and the Edinburgh strain in which the penetrance of abnormal behaviour has declined to about 1%. Breeding experiments suggest that the differences are largely due to differences in the genetic backgrounds which modify foetal susceptibilities to the teratogenic effects of high histidine levels. High susceptibility appears to be dominant over low susceptibility in the present strains. There appears to be no interaction of maternal histidinaemia with the dreher mutation which is considered to induce inner ear malformation as a result of an early neural tube abnormality.

Kimura used the heterozygosity and the number of low-frequency alleles to estimate that about 14% of mutations are selectively neutral. The method is shown to be subject to biases and to disruption due to bottleneck effects. Let deleterious alleles have selective disadvantage, s, compared with neutral alleles and let Ne denote the effective diploid population size. The estimator, , of the proportion of neutral alleles is positively biased if (roughly) 4NeS < 25 or if 4Nes > 200. In the former case, one cannot adequately detect the different influences of deleterious and neutral alleles, whereas in the latter case, deleterious alleles will rarely appear in the sample. These difficulties cause the biases in , and are likely to cause similar biases for any estimation method based solely on allele frequencies. There is substantial sampling variability in in cases of practical interest, when data from 11 loci, or even as many as 31 loci, are pooled. If there has been a recent contraction in population size, will be positively biased, often yielding values greater than 1 or even being infinite. But after a recent expansion in population size, the heterozygosity will not have made as quick an increase and will be negatively biased. Population expansion alone can produce values close to those observed by Kimura, even if all alleles are neutral. In an appendix, a new method for simulating samples of neutral and deleterious genes is described.

Genet. Res., Camb. (1987), 49, pp. 11–18

A latitudinal cline in P–M gonadal dysgenesis potential in Australian Drosophila melanogaster populations

Figures 1 and 2 have been interchanged with their legends. Thus the maps shown as Fig. 2 belong to the legend of Fing. 1, and should be labelled Fig. 1, and vice versa.

Genet. Res., Camb. (1986), 47, pp. 83–91

Structural Genes for Phosphatases in Aspergillus nidulans

A labelling error caused nimD-4 to be substituted for nimQ-20. The nim locus shown in Fig. 3 (p. 88) is nimQ not nimD. The genotypes of strains given in the legend to Fig. 3 should read nimQ-20 in place of nimD-4.