The genes coding for the 18s and 28s ribosomal RNA (rRNA) are present on both the X and Y chromosomes of D. melanogaster at a site known as the bobbed locus. Exchange was observed in males between a normally orientated X and Y chromosome (Dp(1; 1) scv1 and BSY y31d) with a frequency of 0·079%. One-quarter (7 in 27) of these exchange products between two + chromosomes which both carried sufficient rRNA genes for a bb+ phenotype exhibited a bb phenotype. Evidence is presented that one-half, and possibly all, of the exchanges involved the repetitive bb genes. These results together with those reported by Palumbo, Caizzi & Ritossa (1973) imply that the repeated bb genes of either (or both) the X or Y chromosome are not arranged with uniform polarity and, further, that spermatogonial exchange between the X and Y chromosomes may be restricted to the bb loci.

A method is proposed for estimating effective population size (N) from data on linkage disequilibrium among neutral genes at several polymorphic loci or restriction sites. The efficiency of the method increases with larger sample size and more tightly linked genes; but for very tightly linked genes estimates of N are more dependent on long-term than on recent population history. Two sets of data are analysed as examples.

Transcription of X chromosomal DNA has been examined autoradio-graphically in various 1X2A and 2X2A normal larvae and 1X2A (+ X fr) and 2X2A (+ X fr) segmental aneuploid larvae of species Drosophila melanogaster. The segmental aneuploids contained duplications for the segment 9A–11A and 15D–ISA of the X chromosome. Results show that in the aneuploid male containing 9A–11A duplicaton both the homologous segments involved in the aneuploidy are autonomously hyperactive; their combined activity, measured by X/A grain ratio, is found to be nearly 70% more than the activity in normal male and about 100% more than that in diplo-X female. In the aneuploid female, containing the aneuploid segment 15D–18A and having three doses of the segment of the X chromosome, the activity was over 100% more than the diplo-X activity. The per gene dose activity for the two segments in the aneuploid male and female, respectively, is also significantly higher than their male and female counterparts. The possible role of lack of contiguity of the genetic segments and an intra-nuclear variation has been ruled out by appropriate analysis. We, therefore, interpret these findings to be due to an autonomous expression of the X linked compensatory genes, resulting from a primary modulation in the organization of the entire X chromosome. The autosomal signal then renders the individual genetic locus hyperactive.

The Tcp-1 gene is located within the t complex and codes for a major testicular cell protein called p63/6.9. All wild-type chromosomes carry the Tcp-1b allele which codes for a basic form of this protein, while all complete t haplotypes carry the Tcp-1a allele which codes for an acidic form of this protein. It is not clear whether the Tcp-1 gene is associated with phenotypic effects of t haplotypes on embryogenesis and/or spermatogenesis, since the genetic basis for these effects is extremely complex. The elegant analysis of Lyon & Mason (1977) has allowed the identification and separation of a family of genetic factors which interact to produce the observed phenotypes associated with various combinations of t haplotypes. The data summarized in this report indicate that the Tcp-1a locus is separable from all of the identified t haplotype factors except for one; a complete correlation has been obtained between Tcp-1a and a proximal t haplotype factor which is involved in effects on transmission ratio distortion. Two other novel points emerge from this analysis. First, it appears that the tail interaction factor and the proximal sperm factors represent distinct genetic loci. Second, the accumulated data lead to the proposal that the TOrl chromosome carries a short segment of t haplotype chromatin containing Tcp-1a and proximal sperm factors involved in transmission ratio distortion and sterility.

Staphylococcus aureus M4 has chromosomal resistance to streptomycin, plasmid-borne resistance to penicillin and tetracycline and probably chromosomal inducible erythromycin resistance. It also has constitutive erythromycin resistance which is unstable and linked to kanamycin and lincomycin resistance and the ability to produce a diffusible pigment. Variants have been isolated which have stable kanamycin, lincomycin and constitutive erythromycin resistance and these do not produce the diffusible pigment. In transduction experiments kanamycin, lincomycin and constitutive erythromycin resistance were always co-transduced together with streptomycin resistance. The transduction frequencies were approximately 100 times higher with the stable variants compared with the parent. The transductants, irrespective of the donor used, all had stable resistance and did not produce the diffusible pigment. Although transduction with UV-irradiated transducing lysates was characteristic of a plasmid, no corresponding plasmid DNA has been detected.

Mice selected for large size show increases in both food intake and efficiency, and small mice show decreases in both. This is true whether the comparisons are made at the same age or at the same weight. Food intake and efficiency contributed more or less equally to the responses to selection for growth. Mice seem to regulate their food intake to a certain level of energy. On suspension of a period of food restriction, mice ate the same amount as others of the same strain that had not been restricted, and which were bigger. At the same time, they converted it more efficiently than the mice which had been full-fed throughout, because of a linear negative association between efficiency and body weight. Thus, following restriction, mice eat as much as bigger mice of the same age, and convert it as efficiently as younger mice of the same weight. The product of these two effects gives rise to rapid (compensatory) growth.

A comparative study of two male recombination factors (31. 1 MRF and 23. 5 MRF) isolated from the same Southern Greek natural population, revealed specific differences in their activities. 23. 5 MRF induces female sterility due to atrophie ovaries at a wide range of temperatures while 31. 1 MRF does so only at high temperatures. The gross morphology of the atrophie ovaries was the same and unilaterally affected pairs were found in the F1 of crosses with both 23. 5 and 31. 1 MRF. Furthermore, 23. 5 MRF induces: (a) lower frequencies of abnormal anaphases I and II than 31. 1 MRF, (b) higher frequencies of ‘double crossovers’ resulting from deficiences or duplications, (c) large clusters of recombinants, suggesting premeiotic origin and (d) cases where one of the non-recombinant phenotypes was not produced. Such cases have never been observed with 31. 1 MRF. Moreover, the cytoplasm of the Cy L4/Pm strain that suppresses 31. 1 MRF does not affect the activities of 23. 5 MRF. Hypotheses to explain the different behaviour of the two factors are presented and discussed.

Segregation-distorting t-sperm show a specific increase in N-acetylglucosamine: galactosyltransferase activity over wild-type (+/+) due to a deficiency of a wild-type galactosyltransferase inhibitor (Shur & Bennett, 1979). Eight other enzymic activities are indistinguishable between +- and t-sperm suspensions. In this study, three additional points are analysed. First, galactosyltransferases are assayed on sperm homozygous for a semilethal haplotype (tW2/tW2), relative to heterozygous (+ /tw2) and wild-type (+/+) controls. tW2/tW2 assays circumvent the +-sperm inhibition of t-sperm galactosyltransferases that occurs in heterozygous + /t-assays and show that t-sperm are actually four times as active as wild-type. Second, sperm which are compound heterozygotes for two complementing lethal t-haplotypes (tlx/tly), have nearly twice the theoretical enzyme level of tlx/tly sperm. Thus, in either homozygous (tW2/tW2) or double heterozygous (tlx/tly) form t-haplotypes act synergistically on sperm galactosyltransferase activity.

Third, and most interesting, sperm bearing either recombinant, viable t-haplotypes (+/tv, tvx/tvy), or one of three dominant T/t-complex mutations, were assayed to determine which portions of the T/t-complex are responsible for elevated galactosyltransferase activity. Results show that sperm bearing recombinant, non-segregation-distorting, viable tv-haplotypes no longer show elevated transferase activity. Therefore, the elevated t1-sperm galactosyltransferase activity strictly correlates with the increased transmission frequency of t1-sperm. These studies strengthen further the hypothesis that sperm surface galactosyltransferases are involved in egg binding during fertilization, and that t1-sperm segregation-distortion results, at least in part, from increased galactosyltransferase activity.

Aggregation chimaeras were made from embryos of strains of mice selected for large and small body size and of unselected controls. The strains were combined in pairs marked by albino coat colour and by allo-zyme variants at the Gpi-1 locus. The proportion of cells derived from each component was scored visually in the coat melanocytes and by electrophoresis in ten other organs or tissues (blood, liver, lung, spleen, spinal cord, brain, pituitary, kidney, adrenal and testis). The object was to find out how body weight is related to cell proportions in the body as a whole and in the separate organs. Individuals varied widely in their mean cell proportions but there were significant differences between organs within individuals. Body weight was linearly related to the mean cell proportions which accounted for most, or possibly all, of the chimaeric variance of body weight. No one of the organs studied could be identified as being solely responsible for growth control, or as having a predominant influence on growth. The weights of some organs were probably influenced to a small extent by their own cell proportions independently of the individual's mean, but the differences of body weight were too great to be accounted for by the summation of localized effects on organs. The mean cell proportion, averaged over individuals, was close to 50%, proving that there was no tendency for cells from the larger component to outgrow those from the smaller. It is concluded that growth control must be systemic, but it was not possible to decide whether the systemic effect comes from some particular organ not studied, or is in some undefined way the consequence of the cell proportions in the body as a whole. There was some evidence, though it was inconclusive, that chimaeras show ‘heterosis’ for body weight.

The resolution of antibiotic-CsCl gradients enabled an examination of the satellite DNAs in the nuclear DNA of Drosophila simulans. Of the eight distinct satellite DNAs which were detected, four band at almost the same buoyant density in CsCl but can be resolved in netropsin sulphate-CsCl gradients. Each consists of a repeated sequence which, in five of the satellites, is shown to be arranged in tandem for long regions of the chromosomal DNA. One satellite (1·697 g/ml in CsCl) contains repeated sequences interspersed with other sequences. The satellite DNAs were compared with the satellite DNAs known to be present in the sibling species, D. melanogaster. The two species have different overall complements of satellite DNAs, but one satellite (1·672 g/ml) may be identical.

Electrophoretic surveys for nine species of Drosophila have been summarized in terms of the relative contribution to heterozygosity of each of ten gene frequency classes, the mean frequency of heterozygotes within subpopulations, and the degree of genetic divergence between subpopulations. It has been shown that the neutral model proposed by Kimura, and modified by Ohta to include the accumulation of slightly disadvantageous mutations, is capable of explaining all features of the data. The consistent difference between group I and group II enzymes can be explained by a difference in the average intensity of selection against mutational variants in the two groups. A highly significant difference between the temperate and tropical species in the distribution of heterozygosity appears to be due to the smaller effective breeding population sizes in the case of the temperate species.

An electrophoretically detectable variant of acid α-glucosidase has been found in SM/J mice. This variant is attributable to excess sialylation of the enzyme and is determined by a gene, alpha-glucosidase processing, Aglp, on chromosome 17. In addition, as also reported by Potier, Lu Shun Yan & Womack (1979), SM/J mice are relatively deficient in neuraminidase and it appears that the low level of this enzyme in SM/J is determined by an autosomal codominant gene, neuraminidase-1, Neu-1. Preliminary data indicate that Neu-1 is also on chromosome 17. It seems probable that the several processing genes Apl, Aglp and Map-2 which are all closely linked on chromosome 17 are one and the same, a gene Neu-1 coding for neuraminidase.

Eleven catabolic markers have been located on the chromosome of Pseudomonas aeruginosa PAO using FPS-mediated conjugation and G101 transduction. Most of these markers are located in the region 20–35 min, and the remainder in the region later than 60 min. Four chu genes concerned in the sequential degradation of choline to glycine are closely linked.

Previous studies have shown that the mouse X chromosomal locus, Xce, which causes non-random X chromosome inactivation, is closely linked to the Is(X; 7)Ct X-autosome translocation. This has placed it either near Ta on one side of the breakpoint or near jp on the other. Linkage tests with Movbr and Ta now demonstrate that the locus in fact lies close to Ta. The data also provide genetic evidence which establish that the C3H/HeH X chromosome carries the Xcea allele of this gene and the JU/FaCt and C57BL/GoH X chromosomes carry the Xceb allele, and further suggest that the X-linked modification of the heterozygous phenotypes of X-linked genes observed by various other investigators are all attributable to differences at the Xce locus. Evidence of a maternal influence upon Movbr phenotypes is also presented. This appears to operate independently of the X-inactivation process, probably through an effect of differing levels of copper in the milk in early life upon the mutant coat colour in the young.

Selection was carried out in mice for concentration of thyroxine hormone (T4) in plasma of males at 11 weeks of age over seven generations. Selection was practised for high level in two replicate lines and for low level in two replicate lines, and there was an unselected control. There was a response in both directions, and the divergence of 12·4 ng/ml observed in generation seven was equivalent to about 20% of the base population mean or nearly one phenotypic standard deviation. The realised heritability was 9%.

Plasma thyroxine level had a repeatability of 0·54 when two measurements were made 24 h apart. The responses made at 11 weeks in males were also evident in both males and females at 5 weeks. Plasma tri-iodo thyronine (T3) concentrations showed a correlated response almost as large, relative to the mean level, as that in T4.

Positive correlated responses were observed in total weights of the litter at 12 days, and in individual weights at 3, 6 and 9 weeks, the responses in the early weights being greater relative to their mean. The results suggest that the correlated weight changes were due to genetic responses in maternal characteristics, probably milk production, rather than individual growth.

Interest in the selection of mutations affecting L-proline catabolism in Aspergillus nidulans is heightened by the involvement of one of the very few examples of a cluster of functionally related genes in an eukaryote and by an increasing awareness of the biological phenomena in which proline and proline catabolism participate. The sasA-60 (semialdehyde sensitive) mutation in A. nidulans results in toxicity of catabolic precursors of L-glutamic γ-semialdehyde (or its internal Schiff base L-Δ1-pyrroline-5-carboxylate) and succinic semialdehyde, apparently without affecting the catabolic pathways concerned. As sasA-60 is unlinked to the prn gene cluster, specifying the gene products necessary for L-proline catabolism and as L-proline, a precursor of L-glutamic γ-semialdehyde, is highly toxic to sasA-60 strains, this forms the basis of a powerful positive selection technique for obtaining a number of types of prn mutations. Many of these prn mutations can be directly classified according to the gene product(s) affected on the basis of growth phenotype with respect to L-arginine and L-ornithine utilization, proline-dependent resistance to certain toxic amino acid analogues and effect on supplementation of proline auxotrophies. The availability of both a positive selection technique and an extensive nutritional screening system has enabled the identification of fourteen spontaneous deletion mutations, recognized as extending into the prnB gene, specifying the principal L-proline permease, and into at least one other prn gene. These deletion mutations have been partially characterized both genetically and biochemically. In particular their use has greatly facilitated fine-structure mapping of the prn cluster and aided studies of the regulation of prn gene expression.

The relationship between locus variability and genetic identity is analysed in pooled data from a collection of Drosophila and vertebrate allozyme surveys. For vertebrates the analysis provides evidence that loci with high expected heterozygosity diverge at a faster rate than loci with low heterozygosity in comparisons involving pairs of populations and pairs of species. This relationship is not observed in comparisons of Drosophila species pairs.

Yeast cells contain many copies of mitochondrial (mit) genomes. The question we tried to answer was how mit− mutations occurring in one genome as a result of mutagenic treatment might yield homoplasmic mutant cells. Three processes were considered. First, that these cells originate by segregation of mutant and standard alleles during cell division. Secondly, that they originate through intracellular selection, for which cell division is not required. Thirdly, that recombination involving the mutant and standard alleles is non-reciprocal and unidirectional mit+ → mit− so that the mutant allele is spread into the entire population of mitochondrial genomes within a cell, thus making it homoplasmic mit−. The results indicate that the first process, although efficiently producing homoplasmic cells from heteroplasmic zygotes (for review see Birky, 1978), seems to play only a minor, if any, role in producing homoplasmic mutant progenies from mutagenized cells. The most important is the second process, that is, intracellular selection occurring in cells which have one or a few genomes carrying mit− mutations, while the remaining genomes are irreversibly damaged. The third process, unidirectional mit+ → mit− conversion, does not seem to play any part.

Genetic analysis of 12 mutants of Escherichia coli K12 defective in D-alanine dehydrogenase showed that alnA and dad are alternative names for the same locus. dad was shown to be a single gene which codes for a protein of 55000–60000 mol. wt. Study of thermosensitive mutants of dad indicated that its product is a structural component of D-alanine dehydrogenase. The regulatory gene alnR was shown to be involved in positive control of dad expression. This was concluded from (i) the absence of constitutive strains among Dad+ revertants of alnR– mutations, (ii) the trans dominance of alnR+ to alnR–, and (iii) the failure to isolate fully constitutive strains by any means. To obtain a uniform nomenclature it is proposed to re-name dad as dadB and alnR as dadQ.

This report examines several issues bearing upon intragenic recombination in higher eukaryotes. The fine structure data accumulated in our analysis of the genetic organization of the rosy locus in Drosophila melanogaster. Firstly, we confirm that a conversion event has a markedly less than 50% probability of resulting in flanking marker exchange, a finding consistent with more recent analyses of the available Saccharomyces data (e.g. Fogel et al. 1978). As reported earlier, co-conversion of recombinationally separable sites within the rosy locus occurs (McCarron, Gelbart & Chovnick, 1974). In this report, we demonstrate that the frequency of co-conversion is inversely proportional to the distance between co-converting sites. As in fungi, real conversion frequency differences are observed among rosy mutant alleles, and the data suggest that there may be a relationship between allele conversion frequency and map position. Unlike Neurospora and Saccharomyces, only one flanking marker exchange class is recovered from any given mutant heteroallele recombination experiment. In this respect, the Drosophila system resembles Aspergillus. As in Neurospora and Saccharomyces, rosy locus intragenic recombinants associated with flanking marker exchange exhibit interference with crossing over in adjacent regions, while no interference is seen among recombinants exhibiting parental flanking markers. Finally, experimental results are discussed which demonstrate the occurrence of postmeiotic segregation in Drosophila. These analogies between Drosophila and fungi provide further evidence in support of the notion that eukaryotes share common molecular mechanism(s) of meiotic recombination.