The transmission ratio distortion seen in males heterozygous for a mouse t-complex has been explained on the basis of trans-acting distorter genes, having a harmful effect on a responder gene. The t-complex form of the responder is relatively resistant to these harmful effects and hence is preferentially transmitted. Animals homozygous for the t-complex responder would be expected to show equal transmission of the two homologous chromosomes, but this is not always so. Studies described in this paper have shown differences among complete t's in their transmission when opposite a constant responder carrying partial t-haplotype. In addition, the proximal partial haplotypes th49 and tw18, both derived from tw5 but of different lengths, behave differently when opposite a responder. The three central partial haplotypes, tlowH, tlow2H and tlow3H, also differ, in that tlow3H shows lower transmission than tlowH or tloW2H when opposite either wild-type, or another responder, or distorter genes. These results can be explained either on the basis of differences in the responder region of various haplotypes, including the possibility of varying numbers of copies of the relevant sequences, or on the basis of differences in cis-acting (as opposed to trans-acting) distorter genes.

A simple method is given to compare the relative fitnesses of various populations of one species when they compete with another species. Populations of Drosophila psevdoobscura polymorphic for the chromosomal inversions CH and AR are superior to monomorphic populations CH or AR when they compete for the available resources with D. serrata.

Two substrains of the inbred mouse strain 101, maintained at Harwell and at Neuherberg, and designated 101/H and 101/E1, differed at five of the eight genetic loci tested and it seems very likely that one of these substrains has been genetically contaminated. The available evidence suggests that 101/E1 is probably the contaminated substrain.

1. Improved methods for the culture and preservation of Physarum polycephalum amoebae have been developed.

2. Strains of amoebae have been isolated which are stably resistant to 4, 8 or 16 μg./ml. actidione.

3. Sensitivity vs. resistance to 4 μg./ml. actidione is probably controlled by a single pair of alleles at a locus unlinked to the mating-type locus.

4. Plasmodia homozygous or heterozygous for the allele determining resistance at this locus are no more resistant to actidione than plasmodia homozygous for the allele determining sensitivity.

The mutation rate at seven specific loci was measured among the offspring of male and female mice exposed as 17½-day-old foetuses to 200 r. X-rays. In the female series the mutation rate was lower, by a factor of about four, than the comparable adult rate; in the male series the mutation rate was lower but not statistically significantly lower than in adults.

When the technique of saturation mapping is employed to estimate the number of loci in a distinct chromosomal region, there is always the possibility that some loci will not be detected. If the number of mutants per locus follows a Poisson distribution, the number of mutationally silent loci can be estimated. This paper describes a method for fitting such data to a Poisson distribution truncated at the zero class and a method for estimating the number of mutationally silent loci. The use of these methods is demonstrated by their application to some published data.

Models of the macronucleus in Paramecium tetraurelia which assume known levels of ploidy and random segregation of subunits smaller than a haploid set at both fission and macronuclear regeneration (MR) are not consistent with the hypothesis that senescence is due to aneuploid imbalance. Either senescence has some other basis or there is a mechanism for regular distribution of subunits at MR. Random segregation models for fission and MR are consistent with most data on survival and heterozygote stability, but if the ploidy level is 860 they fail to account for the data of Nyberg (this volume). Since the ploidy level may be higher than 860, models of random segregation cannot be ruled out for Paramecium. Models of the macronucleus in hypotrichs which assume randomly segregating chromosome fragments are consistent with data on survival and on stability of heterozygous genotypes at fission.

In this study we estimate the frequency at which P-element insertion events, as identified by in situ hybridization, generate lethal and mild viability mutations. The frequency of lethal mutations generated per insertion event was 0·004. Viability dropped an average of 1% per insertion event. Our results indicate that it is deletions and rearrangements resulting from the mobilization of P elements already in place and not the insertions per se that cause the drastic effects on viability and fitness observed in most studies of P–M dysgenesis-derived mutations. Elements of five other families (I, copia, 412, B104, and gypsy) were not mobilized in these crosses. Finally, we contrast the density of P elements on the X chromosome with the density on the four autosomal arms in a collection of thirty genomes from an African population. The relative number of P elements on the X chromosome is too high to be explained by either a hemizygous selection or a neutrality model. The possible reasons for the failure to detect selection are discussed.

The effects of mutation on mean and variance of response to selection for quantitative traits are investigated. The mutants are assumed to be unlinked, to be additive, and to have their effects symmetrically distributed about zero, with absolute values of effects having a gamma distribution. It is shown that the ratio of expected cumulative response to generation t from mutants, , and expected response over one generation from one generation of mutants, , is a function of t/N, where t is generations and N is effective population size. Similarly, , is a function of t/N, where is the increment in genetic variance from one generation of mutants. The mean and standard deviation of response from mutations relative to that from initial variation in the population, in the first generation, are functions of . Evaluation of these formulae for a range of parameters quantifies the important role that population size can play in response to long-term selection.

Genet. Res., Camb. (1987), 50, pp. 17–21

Heterogeneity of human haptoglobin α chains detected by two-dimensional gel electrophoresis

The running title for this article should have been Human plasma haptoglobin α chain heterogeneity

Genet. Res., Camb. (1987), 50, pp. 63–68

Additive variance and average effect with partial selfing

(1) The second line of Table 1 should read

A class of abnormal sex-ratio (SR) condition in Drosophila characterized by the elimination of male zygotes is caused by infection with maternally transmitted SR-spirochaetes. A given spirochaete strain, WSR, was shown to have an associated DNA virus, spv-2, in a latent condition. This virus is induced to multiply when another DNA virus, previously designated spv-1, infects WSR spirochaetes; spv-1 is normally associated with another strain of SR-spirochaetes, NSR, and is in a manifest state. Spv-2 infects and lyses NSR, thus eliminating spirochaetes from fly hosts which, in these experiments, were D. melanogaster.

The elimination of WSR through lysis by spv-1 results in the ‘curing’ of the SR-condition in the host flies. However, the elimination of NSR by spv-2 does not lead to the immediate elimination of the SR-condition in the host. A hypothesis is presented in favour of the view that a substance, androcidin, is produced by SR-spirochaetes and that this substance is actually responsible for the death of male zygotes. NSR may produce a more potent androcidin than WSR.

The parental origin of 3 de novo X-autosome translocations in females with Duchenne Muscular Dystrophy (DMD) was studied by means of methylation analysis using the X-linked probe M27ß. In all three the translocation was found to be paternal in origin. The parental origin of X-autosome translocations in females with and without DMD is compared with other structural abnormalities of the X and with autosomal translocations.

An experiment was carried out to test whether two laboratory cage populations of Drosophila melanogaster from different origins (Kaduna and Pacific) differed in the genes for sternopleural bristle number. The means, variances and heritabilities of the two populations and the synthetic formed from crosses between them were very similar.

Selection for low bristle number was practised in small replicate lines, six of each pure population and nine of the synthetic. On average, Pacific responded to selection rather more rapidly than either Kaduna or the synthetic, but there was little difference in the limit achieved.

Crosses between replicates within populations were made and selection continued, and these lines subsequently crossed between populations and reselected. Additional response was obtained by this procedure but the crosses between the replicates of the pure and synthetic populations attained similar selection limits.

An analysis of effects of individual chromosomes from the selected lines on bristle number indicated that the contribution of each chromosome to total response was about the same in Pacific, Kaduna and the synthetic.

It is concluded that differences in gene frequency, rather than the presence or absence of particular alleles, are mainly responsible for the differences observed between the populations.

The chromosomal lac region of the coliform bacterium Klebsiella M5al was cloned into the multicopy plasmid pBR322 to give pHE7 and pHE8. pHE8 contains 12·6 kb of M5al DNA, including its complete lac operon, and pHE7 contains 2·5 kb of M5al DNA and includes the complete lac Y gene and a small segment of lacZ. The M5al operon has the same gene order as the Escherichia coli lac operon. The lac genes of the Lac plasmid of Klebsiella V9A were cloned into pBR322 to give pHE1 and pHE2, of approximately 39 and 43 kb. Both plasmids were unstable in an E. coli RecA- strain, in contrast to the stability of pHE8. Polyacrylamide gel electrophoresis tests suggested that the M5a1 β-galactosidase monomer is about 5% longer, i.e. has about 50 more amino acids, than that of the E. coli Z gene. Tests made on the enzymes coded by the lac operons of M5a1, another Klebsiella strain (V9A) and its resident Lac plasmid, and several Lac+ Enterobacteria, led to the conclusion that only Escherichia coli among the Enterobacteria contains an active lacA gene.