Three acid phosphatase allozyme strains (Acph-1, Acph-2 and Acph-4) of Drosophila virilis show large differences of enzyme activity when examined by means of starch gel electrophoretic technique, Acph-4 strain showing approximately four times the activity of Acph-1 and twice that of Acph-2, as reported previously (Narise, 1976). Crude extract difference between Acph-4 and Acph-1 strains is less than twofold and this compared with larger differences in supernatants. Cell fractionation and density gradient centrifugation demonstrated that the acid phosphatase resides mainly in lysosomes and becomes soluble in part during preparation without structural damage to lysosomes. The solubility of the allozymes from lysosomes was variable among the three strains. ACPH4 allozyme was released in the highest degree. However, the release-rate of other lyso-somalenzymes, such as α-glucosidase, β-galactosidase and β-glucuronidase was similar among these strains. These results suggest that the strain variation in ability of the allozymes to be incorporated into lysosomes is due to the allozymes themselves, not due to alteration in the lysosomes.

We have studied the effects on fitness of allelic variation at three gene loci (Est-5, Odh, and Mdh-2)coding for enzymes in Drosophila pseudoobscura. Genotype has a significant effect on fitness for all six parameters measured (female fecundity, male mating capacity, egg-to-adult survival under near-optimal and under competitive conditions, and rate of development under near-optimal and under competitive conditions). No single genotype is best for all six fitness parameters; rather, genotypes with superior performance during a certain stage of the life-cycle may have low fitness at some other stage, or in different environmental conditions. Heterozygotes are sometimes best when all fitness parameters are considered. There are significant interactions between loci. The various forms of balancing selection uncovered in our experiments may account for the polymorphisms occurring in natural populations of D. pseudoobscura at the three loci studied.

A formal genetic analysis of the heterothallic, colonial green alga Eudorina elegans has been described. Wild-type strains were found to be sensitive to different drugs when grown on minimal agar containing very low concentrations of these drugs. Mutant strains resistant to high concentrations of drugs have been isolated. These are msr-500 (resistant to 500 μg/ml of DL-methionine-DL-sulfoximine), ery-r-100 (resistant to 100 μg/ml of erythromycin) and sr-100 (resistant to 100 μg/ml of streptomycin). The wild-type phenotypes sensitive to these drugs have been designated as mss-500, ery-s-100 and ss-100 respectively. The sr-100 also showed cross-resistance to other antibiotics belonging to the streptomycin group.

On genetic analysis, the msr-500 and ery-s-100 were found to be inherited in a Mendelian way. These alleles are not linked to each other or to the mating type locus. The inheritance of mating type was found to be due to a single gene difference.

The inheritance of ss-100/sr-100 was found to be non-chromosomal and was characteristically uniparental, always transmitted through the female parent. The evidence for the non-chromosomal gene (NC genes) controlling sr-100/ss-100 phenotypes in this organism has been derived from the exceptional zygotes in which the male parent apparently transmits streptomycin resistance to the progeny. Although ultraviolet or gamma-radiation resulted in normal survival curves of the exposed cells, no mutant deficient in any nutritional requirement was isolated.

X chromosomes derived from crosses of inbred P and M Drosophila melanogaster strains that had extreme effects on abdominal and/or sternopleural bristle number in males, were further analyzed to determine their effects in females and to map the loci at which the mutations occurred. Seven lines that had on average 3.9 fewer sternopleural bristles than wildtype in males had average homozygous sternopleural bristle effects of −2·2. The bristle effects were partially recessive, with an average degree of dominance of −0·60. Physical mapping of the sternopleural bristle effects of these lines placed them all at approximately 24·7 cM. These mutations are apparently allelic on the basis of a complementation test, and deficiency mapping indicates they occur within chromosomal bands 8A4; 8C6. In situ hybridization analysis of the sites of P element insertions of these lines suggests that mutations probably resulted from excision of P elements at 8C on the original inbred P strain chromosome. Two additional lines, NDC(19) and DP(146), had reduced numbers of sternopleural and abdominal bristles. NDC(19) males had 9·7 fewer abdominal and 8·6 fewer sternopleural bristles than wildtype. The corresponding homozygous abdominal and sternopleural bristle number effects were −5·8 and −3·8, respectively; with the abdominal bristle effect completely recessive and the sternopleural bristle effect nearly additive. DP(146) males had 6·2 fewer abdominal and 4·1 fewer sternopleural bristles than wildtype, with homozygous abdominal bristle effects of −4·3 and sternopleural bristle effects of −2·0. Abdominal bristle effects of this line were partially recessive whereas the sternopleural bristle effects were additive. Physical mapping showed effects on both bristle traits segregated jointly in these two lines, with the NDC(19) mutation closely linked to y and the DP(146) mutation 0·17 cM from it. Complementation tests and deficiency mapping also indicate the mutations in lines NDC(19) and DP(146) are at closely linked but separate loci within chromosomal bands 1B2; 1B4–6 and 1B4–6; 1B10 respectively, with some epistatic effects. In situ hybridization analysis of sites of P element insertion suggest that the NDC(19) mutation, which may be a scute allele, was probably caused by a P element insertion in the IB region; the DP(146) mutation is also associated with an insertion at IB.

This paper describes the results of assays of male life-history characters in a large outbred laboratory population of D. melanogaster. Lines of flies homozygous for the entire third chromosome and lines of flies carrying two different third chromosomes were assayed for agespecific male mating ability (MMA), age-specific survivorship, male fertility, and body mass. The results of these assays were used to calculate the inbreeding decline associated with each of these traits, the average dominance of deleterious alleles that affect the traits, the genotypic and environmental components of variance for the homozygous lines, and phenotypic and genotypic correlations among the characters. Significant inbreeding decline was found for all characters except the Gompertz intercept and fertility. Early and late MMA show larger effects of inbreeding than any other trait. The inbreeding load for MMA is about the same magnitude as that for egg-to-adult viability, but is substantially less than that associated with total fitness. The estimated inbreeding decline and average dominance of male life-history characters are comparable to estimates for other Drosophila fitness components.

Genome sizes (nuclear DNA contents) were documented spectrophotometrically from individuals of each of nine species of the North American centrarchid (sunfish) genus Lepomis. The distributions of DNA values within and among the nine species were essentially normal and continuous, suggesting that changes in DNA quantity in Lepomis are small in amount, involve both gains and losses of DNA, and are cumulative and independent in effect. Significant differences in mean genome size were found between individuals within populations in all nine species and between species. Nested analysis of variance and comparisons of average genome size difference or distance between individuals drawn from different levels of taxonomic organization revealed that the majority of genome size divergence in Lepomis occurs above the hierarchical level of individuals within populations. The Lepomis data when compared to similar data from North American cyprinid fishes appear to suggest that: (i) genome size evolution in these fishes at least follows a continuous rather than a discontinuous mode; (ii) the general predictions of hypothetical models relating genome size variation as a function of organismal position along adaptive continua may be oversimplified, or not applicable to complex, higher eukaryotes; and (iii) changes in genome size in these fishes may be concentrated in speciation episodes.

Freckled (Frd) is a dominant mutant of D. melanogaster, lethal in double dose, which manifests itself by melanization in the adult stage, while nothing can be noticed in the larva and/or in the pupa. Its localization has been determined at nearly 102 of the second chromosome.

Among the offspring from backcrosses involving Frd, some individuals that do not carry the Frd gene exhibit a weak Frd manifestation in the adult stage, or a stronger one, mostly lethal, in the larval or pupal stage. Weak Frd, indicated as [Frd], is transmitted indefinitely without any recognizable linkage with the chromosomes, although its frequency is influenced by the 1st and, probably, by the 3rd chromosome. No matroclinous transmission has been found. It is concluded that [Frd] is probably controlled by an extrachromosomal entity, not located in the cytoplasm. The possible relationships between Frd and [Frd] are discussed.

Twenty autosomal dominant cataract mutations were detected among the offspring of male mice irradiated with γ- or X-rays. The single or fractionated doses ranged from 5.34 to 10.2 Gy. The phenotypic manifestation and penetrance of the mutations as well as fertility and viability of the mutants were studied by extensive breeding. Manifestation of 4 mutations was limited to the lens. Sixteen mutations were characterized by multiple ocular anomalies, of which 4 mutations also affected other organs of the body. Seventy per cent of the mutations caused severe opacity of the lens or lens and cornea. Homologous hereditary diseases in man would be juvenile cataracts with serious impairment of vision or blindness. Expressivity of the lens opacities was almost constant whereas the accompanied defects varied with respect to their severity in different individuals as well as in eyes of an individual. Phenotypic differences dependent on the genetic background could not be observed. Fourteen mutations were classified as mutations with complete penetrance without any effect on viability and fertility of heterozygotes. Four other mutations were shown to be fully penetrant but the viability of the heterozygotes was impaired. Two mutations had incomplete penetrance with no viability or fertility effects. Of the 14 mutations with complete penetrance and normal viability and fertility 6 were shown to be homozygous viable, 1 semi-lethal and 7 lethal.

1. The loss of mu 540, mu 138, and kappa 51 following the loss of the dominant genes required for their maintenance was studied. With mu 540 and mu 138 the loss usually occurred within 4–7 cell generations, but occasional cells with mu were found as late as generation 12 with mu 540 and generation 17 with mu 138. Kappa 51 was lost between 5 and 60 fissions in different clones. The variability in time of loss remains unexplained.

2. No trail of inheritance of resistance to specific kappa killing comparable to the trail of inheritance reported for mu 540 by Gibson & Beale (1962) was found.

3. No loss of kappa 51, mu 540, mu 138, or mu 130 was found following treatment of paramecia with RNase.

4. Didinium nasutum was shown to be able to acquire and maintain kappa 51 when it could not possibly have acquired any RNase-sensitive metagons from paramecia.

5. These results show that the metagon hypothesis cannot be accepted without a number of ad hoc and at present untestable assumptions.

We identify a fixed species difference in the relative concentrations of the cuticular hydrocarbons 2-methyl hexacosane and 5,9-pentacosadiene in Drosophilapseudoobscura and D. persimilis, and determine its genetic basis. In backcross males, this difference is due to genes on both the X and second chromosomes, while the other two major chromosomes have no effect. In backcross females, only the second chromosome has a significant effect on hydrocarbon phenotype, but dominant genes on the X chromosome could also be involved. These results differ in two respects from previous studies of Drosophila cuticular hydrocarbons: strong epistasis is observed between the chromosomes that producethe hydrocarbon difference in males, and the difference is apparently unrelated to the strong sexual isolation observed between these species.

Position effect variegation has been studied in female mice heterozygous for the flecked X-autosome translocation, T(7; X)Ct. Some of these carried the spotting gene (s) which clarifies the variegated patterns. Others carried a second X-autosome translocation, T(X; 16)16H, which suppresses the randomness of X-chromosome activity.

It was found the position effect variegation stems primarily from early occurring events which lead to the formation of clones of cells with different phenotypes. In this respect the phenomenon appears to parallel that found in Drosophila. However, in the mouse, late-occurring events are also found which can only be readily accounted for by the reactivation of previously inactive loci. They occur, not only during foetal development, but throughout the life-time of the animals and in a manner which suggests they derive from a progressive retreat of the inactivating influence of the heterochromatic X chromosome back along the attached autosome towards the breakpoint. It is proposed that the early occurring events do not lay down fixed programmes of gene suppression, as proposed for Drosophila, but that, like the later-occurring events, they represent the reactivation of previously inactivated loci. The possibility that this might also be true for Drosophila is discussed.

The study also provided evidence favouring the view that the X-chromosome controlling element, Xce, modifies the heterozygous phenotypes of X-linked genes by biasing the randomness of the X-inactivation process, rather than by operating through cell selection mechanisms. The data also support and extend Mintz's (1967) concept of pigment pattern differentiation.

Retarded development of females (Symbol: Rf) has arisen spontaneously as a new trait in a chromosome mutant strain, which has an autosome fused to the original W chromosome. Female imagines with this trait emerge 1–3 weeks later than the males, due to retarded larval development. The proportion of female imagines is low. Rf is maternally inherited, it is neither expressed in nor transmitted through males. The evidence suggests that it is a dominant or epistatic factor on the autosomal part of the W chromosome-autosome fusion.