The Uq transposable element is one of two transposable elements consistently found in maize (Zea mays L.) populations. Populations developed from two independent recurrent selection programs initiated in the Iowa Stiff Stalk Synthetic (BSSS) maize population were tested for the frequency of Uq transposable elements to determine how Uq frequency has changed with cycles of recurrent selection. In the first programme, 13 cycles of half-sib and S2 progeny recurrent selection [BSSS(S)C13] have been completed and 10 of the 13 cycles were assayed for active Uq elements. In the second programme, 11 cycles of reciprocal recurrent selection [BSSS(R)C11] have been completed and five of the 11 cycles were assayed for active Uq elements. The frequency of Uq was different for the two recurrent-selection programmes. The percentage of plants containing active Uq elements increased from 19% (BSSS) to 91% [BSSS(S)C13] at a linear rate after 13 cycles of half-sib and S2 progeny recurrent selection, whereas the percentage of plants containing active Uq elements decreased from 19% (BSSS) to 0% [BSSS(R)C11] after 11 cycles of reciprocal recurrent selection, with extinction of the Uq element occurring between the fifth and sixth cycles of selection. Our data suggest that the increase in frequency of Uq with half-sib and S2 progeny recurrent selection was predominantly due to random genetic drift coupled with a selective advantage possibly associated with a region of the genome linked to Uq. Neither replicative transposition or chromosome assortment and segregation can be invoked to explain the change in frequency of Uq in these populations. The extinction of Uq after reciprocal recurrent selection was best explained by random genetic drift.

Several genetic mosaics for larval body marking of the silkworm, Bombyx mori, have been induced by X-ray irradiation. It is hypothesized that the occasional loss of chromosomal fragments carrying the genes for body marking during development may give rise to this type of mosaicism. Using pulsed field gel electrophoresis (PFGE), we find that a DNA molecule of about 2·5 megabases (Mb) is present in one type of mosaic (mottled striped strains pSm788 and pSm872), and not in any other strain. This DNA fragment hybridizes strongly with some chorion genes which are less than 6·9 cM away from the ps locus, and hence it corresponds to a chromosomal fragment containing genes for both striped marking (ps) and the chorion. In the non-mottled ps strain, the phenotype before X-ray irradiation, no band was detected either on a PFGE gel or after hybridization with the chorion probe. These results suggest that the mottled ps strains carry short chromosome fragments which are lost differentially during cell divisions.

Resistance to the cyclodiene insecticide dieldrin maps to a single gene (Rdl) on the left arm of chromosome III in Drosophila melanogaster (Meigen). The gene was further mapped by the use of chromosomal deficiencies to a single letter sub-region, 66F, on the polytene chromosome. The cross-resistance spectrum of a backcrossed strain lacking elevated mixed function oxidase activity, a common resistance mechanism, was examined. Levels of resistance similar to those found in other insects were found to dieldrin, aldrin, endrin, lindane, and picrotoxinin. Strong similarity of this single major gene with that found in other cyclodiene resistant insects is suggested by its cross-resistance spectrum and chromosomal location, via homology with other Diptera. The significance of major genes in insecticide resistance is discussed.

The experiments reported here are aimed at determining whether mutations deleting the function of the Sex-lethal (Sxl) gene are able to suppress the lethality of X0 clones, induced in females after the time when the state of activity of Sxl is irreversibly fixed by the ratio of the number of X chromosomes to sets of autosomes (X: A). This analysis was carried out by comparing the frequency of induced male clones (X0 constitution) in SxlfLS/ + and Sxl+/Sxl+ females, following irradiation at blastoderm and larval stages. The genotype used in these experiments, however, could also give rise to 2X; 2A cells homozygous for SxlfLS, and such cells would also differentiate male structures. To minimize this possibility, we have constructed a genotype made up of a ring and a rod X chromosome. In such ring-rod females the production of 2X; 2A clones homozygous for SxlfLS is a rather rare event, if possible at all. X0 male clones were produced in both types of females following irradiation at blastoderm stage, while X0 male clones were only observed in SxlfLS/ + females when irradiation took place at larval stage. In this latter case, the only X0 male clones were those that contained the SxlfLS mutation. These results support the idea of Sánchez & Nöthiger (1983) that the X: A signal irreversibly sets the state of activity of Sxl at blastoderm stage, and in addition show that X0 clones generated after that time are viable if they contain a Sxl− mutation. These results are compatible with the idea of Sxl being the only gene that responds to the X:A signal.

A spontaneous mutation ‘tich’ (gene symbol tch) appeared as a recessive mutation in inbred mice of strain A. TL. Homozygotes are rather dumpy mice of approximately normal weight but with short limbs and tail. Skeletal measurements on backcross siblings show that the mandible bones are almost normal but long bones and some parts of the pelvic and pectoral girdles are short. Although tich resembles brachypodism phenotypically it is not linked to agouti, and does not match the description of any other skeletal mutation. There was some evidence for weak linkage with albinism on chromosome 7. The mutation has reappeared amongst the A. TL mice of a UK commercial breeder and may have been accepted as the norm for A. TL amongst some European users of this mouse.

Mutations in the structural genes for triosephosphate isomerase and glyceraldehyde-3-phosphate dehydrogenase activity in the mouse, selected after mutagen treatment, were used to estimate the map distance between the two loci. It is shown that Tpi-1 and Gapd are closely linked on chromosome 6, with a recombination frequency of 0·1±0·1%.

We have examined the effects of major histocompatibility (H-2) haplotypes and genetic background (all loci other than the H-2 region) on hormone-induced ovulation rate in congenic strains of mice. In comparison with the H-2a haplotype, the H-2b haplotype increased hormone-induced ovulation rate 92% on the A/J (A) genetic background. However, H-2 haplotype did not affect hormone-induced ovulation rate on the C57BL/10J (C57) genetic background. The H-2b-linked gene(s) increased hormone-induced ovulation rate on the A/J genetic background largely by (1) enhancing the maturation of follicles in response to pregnant mare's serum gonadotrophin (PMSG) and (2) altering the stages of follicular development which can be induced to ovulate in response to human chorionic gonadotrophin (hCG). The observed effects of H-2 on hormone-induced ovulation rate were not explained by differences in the timing of puberty, the number of follicles present in untreated females, or the incidence of follicular atresia. The effect of genetic background on hormone-induced ovulation rate was much greater than was the effect of the H-2 region. We found that hormone-induced ovulation rate was five- to six-fold higher on the C57 genetic background than on the A genetic background. The C57 genetic background increased hormone-induced ovulation rate by (1) enhancing the induction of follicular maturation in response to gonadotropins and (2) by reducing the incidence of follicular atresia.

The properties of the t haplotypes, specific mutant states of the proximal region of chromosomes 17 in the house mouse, are of continuing interest. One such property is increased transmission of the t haplotype by heterozygous t/ + males to offspring. Using the reciprocal translocation T(16; 17)43H we have constructed males with tertiary trisomy of chromosome 17 (+ T43/+ +/Rb7 + ) carrying the Robertsonian translocation Rb(16.17)7Bnr. Only the progeny of these males which had inherited either T43/ + or Rb7 from their male parent were viable. The segregation patterns in the offspring of t-bearing trisomics were analysed on days 16–18 of embryonic development. It was found that, when the t12 haplotype is in the normal acrocentric (♂♂ + + T43/ + t12 + /Rb7 + +), its presence in the gamete + t12 + / + + T43 does not produce meiotic drive. However, when t6 is in Rb7, meiotic drive was observed: 80% of offspring carried the t haplotype. It is concluded that the meiotic drive is probably inhibited by the presence of a normal homologue of chromosome 17 in the same sperm. Possible mechanisms for the t haplotype effect are discussed.

To evaluate whether sex reversal contributes to sex-ratio imbalance among t6/tw5 double heterozygotes, the cross performed by K. B. Bechtol (Genetical Research 39, 1982, 79–84), T/t6 × T/tw5, was repeated. Significantly more normal-tailed (t6/tw5) females than males were recovered. By contrast, sex ratios were normal among tailless progeny resulting from this cross and among all classes produced by control crosses. Hybridization of a Y-specific DNA probe with genomic DNA from phenotypic females revealed no XY, sex-reversed males. On the genetic backgrounds that generated only moderate transmission distortion of tw5 (81–85%), the overall viability of the doubly heterozygous progeny was only 50% and the sex-ratio skew among this class was strong. However, on a genetic background that displayed extreme tw5 transmission (99%), embryonic viability was more than 80% and the sex-ratio imbalance was weak.

Esterase-27A (ES-27A) was characterized in strain A/WySnA by a cascade of seven bands seen after disc electrophoresis of serum and subsequent staining for esterase. ES-27A catalyses the hydrolysis of thiocholine butyrate and is strongly inhibited by 100 μm tetraisopropyl pyrophosphamide (isoOMPA). Hence, the enzyme was concluded to be a cholinesterase EC 3.1.1.8. A heat-labile form termed ES-27B was represented by strain AKR/Han. From a three-point cross (AKR/Han, A/Wy) and a five-point cross (AKR/Han, SEG/1), the gene order on chromosome 3 was concluded to be centromere–Car-2–Es-26–Es-27–Amy-1–Adh-1.

Data from 23 generations of mice selected for increased and reduced appetite were analysed by Restricted Maximum Likelihood fitting an animal model with litters as additional random effects. Traits considered were food intake between 4 and 6 weeks of age adjusted for 4-week body weight (AFI), the selection criterion, and body weight at 6 weeks (6WW). Selection was carried out within families. A high and a low selection line and a control were maintained in each of three replicates. Analyses were performed for each replicate separately taking subsets of the data spanning different numbers of generations. Overall estimates of heritabilities were 0·15 for AFI, which agreed well with realized heritability estimates, and 0·42 for 6WW. The litter variance, expressed as a proportion of the phenotypic variance, was 0·21 for both traits, yielding intraclass correlations of full-sibs of 0·29 and 0·42, respectively. Similar results were obtained for variances of each trait using univariate and multivariate analyses. From the latter, estimates of correlations between the two traits were 0·46 for additive genetic, −0·19 for litter and 0·31 for residual effects, resulting in a phenotypic correlation of 0·23. Analyses of data from generations 2–7, 8–13 and 14–23 separately showed a marked decrease in genetic variance and heritability in later generations for both traits. Heritabilities of AFI, for instance were 0·24, 0·10 and 0·07, respectively. These changes could not be attributed to the effects of inbreeding or of selection in an infinitesimal model and suggested that some change in variance due to change in gene frequency had occurred during the course of the experiment.

A population genetic model with a single locus at which balancing selection acts and many linked loci at which neutral mutations can occur is analysed using the coalescent approach. The model incorporates geographic subdivision with migration, as well as mutation, recombination, and genetic drift of neutral variation. It is found that geographic subdivision can affect genetic variation even with high rates of migration, providing that selection is strong enough to maintain different allele frequencies at the selected locus. Published sequence data from the alcohol dehydrogenase locus of Drosophila melanogaster are found to fit the proposed model slightly better than a similar model without subdivision.