The often remarkable similarity in structural gene products among related species has led to the hypothesis that species differences may reside largely in changes at regulatory gene loci. This hypothesis assumes that groups capable of speciating have allelic variation at regulatory loci in their natural populations. We have undertaken an analysis of the mode of regulation of the esterase 6 (Est 6) locus in Drosophila melanogaster to determine the nature and extent of regulatory gene variation in natural populations. Analyses of esterase 6 (EST 6) activity among strains carrying the same thermostability variants reveal that significant, specific-activity differences are present. Reciprocal crosses between lines having high and low EST 6 activity show that loci other than the Est 6 structural gene influence EST 6 activity. Analyses of male hybrids from crosses between D. melanogaster and simulans indicate that the X chromosome of these flies affects the expression of the Est 6 locus, resulting in unequal levels of enzyme activity from the two alleles. The effect is sex and tissue specific. Female hybrids carrying the X chromosomes of both species exhibit equal expression of the two Est 6 alleles. We have determined whether natural populations are polymorphic for X chromosomes which affect EST 6 activity by extracting single X chromosomes from wild-collected males and placing these chromosomes in identical genetic backgrounds. Stocks which are otherwise genetically identical but carry independently derived X chromosomes show significant differences in the activity of EST 6. These data suggest that regulatory loci may be commonly polymorphic in natural populations.

Linear functions of Nei's genetic-distance statistic are calculated frequently in the literature of population genetics. Variance estimates for these linear functions are either not presented or incorrectly calculated. Part of the problem stems from the common assumption that distance statistics are independent random variables. This assumption is not generally correct. We describe methods for estimating the variance of linear combinations of genetic-distance statistics. We also suggest a method for constructing confidence intervals on genetic-distance statistics when these values are small (< 0·10) and their distribution deviates substantially from normal.

Previous studies have shown that different alleles of the mouse X chromosomal controlling element locus, Xce, cause non-random X-chromosome inactivation as judged by variegation in the coats of female mice heterozygous for X-linked coat colour/structure genes, or Cattanach's translocation (Is (X; 7) Ct), or the relative activity of biochemical variants of the X-linked enzyme PGK. This paper presents evidence using the Kanda differential staining method on 6½ d.p.c. and 13½ d.p.c. female mouse embryos heterozygous for the marker X chromosome Is (X; 7) Ct and carrying different Xce alleles, that the Xce locus affects the randomness of X chromosome inactivation. Furthermore the fact that a marked Xce effect is demonstrable in female embryos as early as 6½ d.p.c. (i.e. very soon after the initial time of X-inactivation) is strong evidence that the Xce locus exerts its effect by causing primary non-random X-inactivation rather than by cell selection after initial random X-inactivation.

In the fungus Podospora anserina, mutations were selected which relieved the hypersensitivity to paromomycin caused by four suppressors assumed to be ribosomal ambiguity mutations (su1–31, su1–49, su1–60, su2–5). Our first purpose was to isolate new antisuppressor mutations and in fact a new antisuppressor gene, AS7 was uncovered. The AS7–1 mutant displays a pleiotropic phenotype and particularly a sporulation defect. On the other hand, a new su1 mutant was obtained which acts as a suppressor and also as an antisuppressor: it can specifically reduce the suppressor effect of certain su2 mutations. This property of some su1 and su2 mutations was already known. Apart from these mutations probably involved in the control of translational fidelity, six mutations conferring cross-resistance to paromomycin and neomycin were isolated. While four of them are localized in the Pm1 and Pm2 loci previously identified, the two others define a new gene which controls paromomycin and neomycin resistance, Pm3. Strains carrying the Pm3–1 allele are sensitive to temperature at the level of growth and sporulation. The three last mutations which were obtained confer no mutant phenotype when separated from the su1 background. They are closely linked to the su2 locus.

The relationship between chromosome pairing and chromosome fragmentation has been studied in a gene controlled mutant of pearl millet (2n = 14). Premeiotic mitosis, premeiotic cell development and early prophase I are normal without any fragments, which first appear at pachytene. The extent of fragmentation varies from zero to very extreme with two discrete classes of plants, namely those with partial fragmentation and those with multiple fragmentation. A quantitative analysis of bivalent distribution and the distribution of AI bridges in desynaptic and fragmented cells show all of them to be nonrandom events. We suggest that in cells showing partial fragmentation the bridges and fragments result from U-type exchanges at pachytene. The reduced frequency of AII bridges indicates relatively low sister chromatid reunion at pachytene. In multiple fragmented plants numerous minute fragments were seen from pachytene. Despite these anomalies most PMCs complete meiosis but subsequently abort at the pollen grain stage. The mutant gene also causes disturbances in the sequence of meiotic development in the ear and in the synchronous development of PMCs within an anther. It has no effect on the tapetum or on the physiological development of the anther.

In(IL; IR)O Y348 is a pericentric inversion of linkage group I in N. crassa, with a breakpoint between fr and un-5 in the left arm and a breakpoint between ad-9 and nit-1 in the right arm. Approximate breakpoint location was found by tabulating crossovers between the rearrangement and markers in normal chromosome sequence. Inversion structure was verified by marked In O Y348 × In O Y348 crosses. Precise mapping of breakpoints was by duplication coverage. Inversions like O Y348 do not produce progeny with segmental chromosome duplications when crossed to normal sequence, but duplications were produced by crossing it to In(IL; IR)O Y323 (Barry & Leslie, 1982), another standard pericentric inversion, and to T(I → VI)NM103 (Turner, 1977), a translocation to a tip. Each of these rearrangements has a breakpoint within the inverted region of In O Y348. Two duplications from In O Y348 × In O Y323 were converted to normal chromosome sequence by double mitotic recombination. Besides expediting mapping, the technique of intercrossing rearrangements increasingly enables us to make segmental duplications exactly tailored for studying specific included genes.

Seven temperature-sensitive paralytic mutants were recovered from 4544 lines of ethylmethanesulphonate (EMS) treated autosomes in Drosophila melanogaster. These mutants have been designated temperature-induced paralytic (tip). The tip mutations belong to six different genes; four of these, tip-A, Tip-B, tip-C and tip-D are on the second chromosome while tip-E and tip-F are on the third chromosome. This paper describes the paralysing behaviour and genetic localization of the tip mutants.

Selective differences among male Drosophila melanogaster due to differences in ability to compete for mates may often have been under-estimated in the past because, under the test procedure used, females did not represent a limited resource. In the experiment reported here, no difference was detected between inbred and outbred males ‘competing’ to mate with an equal number of females. When the receptive female: male ratio was halved a large reduction in male mating ability due to inbreeding became apparent.

Wild-type Friend murine leukaemia (clone 707) cells and two thymidinekinase-deficient subclones, 707BUE and 707BUF, were compared for sensitivity to killing and mutagenesis by the chemical mutagens, ethyl methane sulphonate (EMS), N-methyl-N′-nitro-N-nitrosoguanidine (MNNG), mitomycin C (MMC), and methyl methane sulphonate (MMS). The two thymidine-kinase-deficient subclones were significantly more sensitive to killing by each of the four chemical mutagens than were wild-type cells. The increased sensitivity to killing by the four mutagens was also reflected in increased mutagenesis (per unit dose of mutagen) to 6-thioguanine resistance. In the light of these results, the significance of thymidine kinase in DNA repair and mutagenesis is discussed.

The linkage of the locus of the major liver protein, Lvp-1, has been established on chromosome 6. Testcross data show the following gene order and recombination percentages:

centromere −Hd−7·4 ±2·4%−Lvp-1−13·2±3·1% −mi

Data from 39 recombinant inbred strains show complete concordance of the Lvp-1 locus and the Lyt-2 locus on chromosome 6.