Variance component analysis of bristle characters in local populations of Drosophila melanogaster.

The genetic variabilities of sternopleural and abdominal bristle numbers existing in local natural populations were assessed. Using second chromosome lines of Drosophila melanogaster extracted from three natural populations in Japan (the Ishigakijima, Ogasawara and Aomori populations), experiments were conducted to estimate the components of genetic variances, additive and dominance variances. The following results were obtained: For both sternopleural and abdominal bristle numbers, the additive genetic variances (sigma 2A) were much larger than the dominance variances (sigma 2D) especially in the southern populations. For example, in the Ishigakijima population, for females sternopleural bristle numbers of the inversion-free chromosome group, the additive and dominance variances were estimated to be 1.255 +/- 0.2034 and 0.0552 +/- 0.0180, respectively. The magnitudes of the estimates of additive genetic variances were nearly equal from north to south. By comparing the additive genetic variances of the inversion-free chromosome group with those of the In(2L)t-carrying chromosome group, it was inferred that sufficient number of generations to achieve the equilibrium state has not passed since the introduction of a single or a small number of the In(2L)t-carrying chromosomes to the Ishigakijima population.     

The Genetic Structure of Natural Populations of DROSOPHILA MELANOGASTER. Xvi. Excess of Additive Genetic Variance of Viability

About 500 second and 500 third chromosomes were extracted, using the marked inversion technique, from the Orlando-Lake Placid, Florida, population. From the experiments using these chromosomes, the following findings were obtained: (1) The frequencies of lethal-carrying chromosomes were 0.37 in the second and 0.55 in the third chromosomes. (2) The size of the population was estimated to be effectively infinite, on the basis of the allelism rate of lethal-carrying chromosomes. (3) The detrimental and lethal loads for viability were, respectively, 0.40 and 0.45 for the second and 0.52 and 0.78 for the third chromosomes. Consequently, the detrimental to lethal load ratio is 0.90 for the second and 0.67 for the third chromosomes. (4) Lethal genes were shown to be deleterious when heterozygous. (5) The average degree of dominance for mildly deleterious genes (viability polygenes) was estimated to be nearly 0.5, although the confidence interval is large. (6) Additive (sigma( 2) (A)) and dominance (sigma(2) ( D)) variances of viability were estimated by using a partial diallel cross method. The results were (see PDF) and (see PDF) for the second chromosomes. (7) Environmental variances of viability were estimated. The result indicates that the heterozygotes are more homeostatic than the homozygotes. The most striking finding is that the additive variance is larger than expected on the classical hypothesis from the detrimental load. Several possible explanations for the discrepancy are offered. The most likely cause, we suggest, is genotype-environment interaction (diversifying selection) acting on viability polygenes. Overdominance is inconsistent with the low dominance variance, and frequency-dependent selection also appears unlikely as an explanation.     

The Genetic Variance for Viability and Its Components in a Local Population of DROSOPHILA MELANOGASTER

Two hundred and ninety second chromosomes extracted from a natural population of Drosophila melanogaster were analyzed to estimate the genetic variance of viability and its components by means of a partial diallel cross (Design II of Comstock and Robinson 1952). The additive and dominance variances are estimated to be 0.009 and 0.0012. Using the dominance variance and the inbreeding depression, the effective number of overdominant loci contributing to the variance in viability is estimated to be very small, a dozen or less. Either the actual number of loci is small, or the distribution of viabilities is strongly skewed with a large majority of very weakly selected loci. The additive variance in viability appears to be too large to be accounted for by recurrent harmful mutants or by overdominant loci at equilibrium with various genetic parameters estimated independently. The excess might be due to frequency-dependent selection, to negative correlations between viability and fertility, or possibly to the presence of a mutator. The selection for viability and fertility, or possibly to the presence of a mutator. The selection for viability at the average polymorphic locus must be very slight, of the order of 10(-3) or less.     

The Genetic Structure of Natural Populations of Drosophila melanogaster. Xx. Comparison of Genotype-Environment Interaction in Viability between a Northern and a Southern Population

In order to examine the operation of diversifying selection as the maintenance mechanism of excessive additive genetic variance for viability in southern populations in comparison with northern populations of Drosophila melanogaster, two sets of experiments were conducted using second chromosomes extracted from the Ogasawara population (a southern population in Japan) and from the Aomori population (a northern population in Japan). Chromosomal homozygote and heterozygote viabilities were estimated in eight kinds of artificially produced breeding environments. The main findings in the present investigation are as follows: (1) Significant genotype-environment interaction was observed using chromosomes extracted from the Ogasawara population. Indeed, the estimate of the genotype-environment interaction variance for heterozygotes was significantly larger than that of the genotypic variance. On the other hand, when chromosomes sampled from the Aomori population were examined, that interaction variance was significant only for homozygotes and its value was no more than one quarter of that for the chromosomes from the Ogasawara population. (2) The average genetic correlation between any two viabilities of the same lines estimated in the eight kinds of breeding environments for the chromosomes sampled from the Ogasawara population was smaller than that for the chromosomes from the Aomori population both in homozygotes and in heterozygotes, especially in the latter. (3) The stability of heterozygotes over homozygotes against fluctuations of environmental conditions was seen in the chromosomes from the Ogasawara population, but not from the Aomori population. (4) From the excessive genotype-environment interaction variance compared with the genotypic variance in heterozygotes, it was suggested for the chromosomes from the Ogasawara population that the reversal of viability order between homozygotes took place in some environments at the locus level. On the basis of these findings, it is strongly suggested that diversifying selection is operating in a southern population of D. melanogaster on some of the viability polygenes which are probably located outside the structural loci, and the excessive additive genetic variance of viability in southern populations is maintained by this type of selection.     

The Genetic Structure of Natural Populations of DROSOPHILA MELANOGASTER. Xi. Genetic Variability in a Local Population

Six hundred and ninety-one second chromosomes were extracted from a Raleigh, North Carolina population, and the following experimental results were obtained: (1) Salivary gland chromosomes of all lines were observed and the number of inversion-carrying chromosomes was 130, among which 76 carried In(2R)NS, 36 carried In(2L)t, 4 carried In(2L)t and In(2R)NS, and 14 carried different kinds of rare inversions. (2) Viabilities of homozygotes and heterozygotes were examined. The frequency of lethal-carrying chromosomes was 275/691 (or 0.398):70/130 (or 0.538) in inversion-carrying chromosomes and 205/561 (or 0.365) in inversion-free chromosomes. The former is significantly higher than the latter. The average homozygote viability was 0.4342 including lethal lines and 0.7163 excluding those, the average heterozygote viability being 1.0000. The detrimental load to lethal load ratio (D:L ratio) was 0.334/0.501 = 0.67. The average viability of lethal heterozygotes was less than that of lethal-free heterozygotes, significantly in inversion-free individuals but not significantly so in inversion-carrying individuals. Inversion heterozygotes seem to have slightly better viability than the inversion-free heterozygotes on the average, but not significantly so. (3) The average degree of dominance of viability polygenes was estimated to be 0.293 +/- 0.071 for all heterozygotes whose component chromosomes had better viabilities than 0.6 of the average heterozygote viability, 0.177 +/- 0.077 for inversion-free heterozygotes and 0.489 +/- 0.082 for inversion heterozygotes. (4) Mutation rates of viability polygenes and lethal genes were estimated on the basis of genetic loads and average degrees of dominance of lethal genes and viability polygenes. Estimates were very close to those obtained by direct estimation. (5) Possible overdominance and epistasis were detected, but the magnitude must be very small. (6) The effective size of the population was estimated to be much greater than 10,000 by using the allelism rate of lethal-carrying chromosomes (0.0040) and their frequency.-On the basis of these findings and the comparison with the predicted result (Mukai and Maruyama 1971), the mechanisms of the maintenance of genetic variability in the population are discussed.     

The Genetic Structure of Natural Populations of DROSOPHILA MELANOGASTER. Xvii. a Population Carrying Genetic Variability Explicable by the Classical Hypothesis

About 400 second chromosomes were extracted from the Aomori population, a northernmost population of D. melanogaster on Honshu in Japan, and the following experimental results were obtained. (1) The frequency of lethal chromosomes was 0.23. (2) The effective size of the population was estimated to be about 3000, from the allelism rate of lethal chromosomes and their frequency. (3) The detrimental and lethal loads for viability were 0.243 and 0.242, respectively, and the D/L ratio became 1.00. (4) The average degree of dominance for mildly deleterious genes was estimated to be 0.178 ± 0.056. (5) Additive (σ²_A) and dominance (σ²_D) variances of viability were estimated to be 0.00276 ± 0.00090 and 0.00011 ± 0.00014, respectively. (6) There was no significant difference in environmental variances between homozygotes and heterozygotes. Using these estimates, we discuss the maintenance mechanisms of genetic variability of viability in the population. The mutation-selection balance explained these experimental results.     

The genetic structure of the Raleigh natural population of Drosophila melanogaster revisited

The Raleigh natural population of Drosophila melanogaster was reanalyzed with special attention to possible dysgenic effects during the extraction of chromosomes. About 600 second chromosomes were extracted from the Raleigh natural population, half in the cytoplasm of wild-caught females (native genetic background) and half in the cytoplasm of the laboratory line, C160(In(2LR)SM1, Cy/In(2LR)bw(V1)) (foreign genetic background). We could not find significant differences between the two extraction schemes in the frequency of lethal second chromosomes (Q = 0.252 for the lines with the negative genetic background vs. 0.231 for the lines with the foreign genetic background) or in the homozygous detrimental (D) and lethal (L) loads (D = 0.210 vs. 0.251; L = 0.287 vs. 0.264). The effective size of the population was estimated to be approximately 19,000, based on the allelism rate of lethal-bearing chromosomes. The homozygous load markedly decreased in the 15 years since a previous study of the same population.     

The Genetic Structure of Natural Populations of DROSOPHILA MELANOGASTER. Xix. Genotype-Environment Interaction in Viability

To investigate whether or not an excess of additive genetic variance for viability detected in southern natural populations of Drosophila melanogaster was created by diversifying selection, genotype-environment interaction was tested as follows. (1) Two karyotype chromosomes were used: 61 second chromosomes with the standard karyotype and 63 second chromosomes carrying In(2L)t. Their homozygote viabilities were larger than 50% of the average viability of random heterozygotes. (2) The effects of two factors (culture media and yeasts) were examined at three levels (the culture media: tomato, corn and banana; and the yeasts: sake, brewer's and baker's). The results of 16 three by three factorial experiments by the Cy method in the same karyotype groups for relative viabilities of homozygotes and heterozygotes elucidated the following findings: (1) there was no significant difference between the two karyotype groups, (2) the variance components of genotype-environment interaction were highly significant, (3) the variance component of heterozygotes was significantly smaller than that of homozygotes. From the experimental findings and previous results, diversifying selection in natural populations acting on viability polygenes to increase the additive genetic variance was suggested. The relation of the present result to protein polymorphism is also discussed.     

The Effects of Spontaneous Mutation on Quantitative Traits. I. Variances and Covariances of Life History Traits

We have accumulated spontaneous mutations in the absence of natural selection in Drosophila melanogaster by backcrossing 200 heterozygous replicates of a single high fitness second chromosome to a balancer stock for 44 generations. At generations 33 and 44 of accumulation, we extracted samples of chromosomes and assayed their homozygous performance for female fecundity early and late in adult life, male and female longevity, male mating ability early and late in adult life, productivity (a measure of fecundity times viability) and body weight. The variance among lines increased significantly for all traits except male mating ability and weight. The rate of increase in variance was similar to that found in previous studies of egg-to-adult viability, when calculated relative to trait means. The mutational correlations among traits were all strongly positive. Many correlations were significantly different from 0, while none was significantly different from 1. These data suggest that the mutation-accumulation hypothesis is not a sufficient explanation for the evolution of senescence in D. melanogaster. Mutation-selection balance does seem adequate to explain a substantial proportion of the additive genetic variance for fecundity and longevity.     

A Building Block Model for Quantitative Genetics

We introduce a quantitative genetic model for multiple alleles which permits the parameterization of the degree, D, of dominance of favorable or unfavorable alleles. We assume gene effects to be random from some distribution and independent of the D's. We then fit the usual least-squares population genetic model of additive and dominance effects in an infinite equilibrium population to determine the five genetic components--additive variance sigma 2 a, dominance variance sigma 2 d, variance of homozygous dominance effects d2, covariance of additive and homozygous dominance effects d1, and the square of the inbreeding depression h--required to treat finite populations and large populations that have been through a bottleneck or in which there is inbreeding. The effects of dominance can be summarized as functions of the average, D, and the variance, sigma 2 D. An important distinction arises between symmetrical and nonsymmetrical distributions of gene effects. With symmetrical distributions d1 = -d2/2 which is always negative, and the contribution of dominance to sigma 2 a is equal to d2/2. With nonsymmetrical distributions there is an additional contribution H to sigma 2 a and -H/2 to d1, the sign of H being determined by D and the skew of the distribution. Some numerical evaluations are presented for the normal and exponential distributions of gene effects, illustrating the effects of the number of alleles and of the variation in allelic frequencies. Random additive by additive (a*a) epistatic effects contribute to sigma 2 a and to the a*a variance, sigma 2/aa, the relative contributions depending on the number of alleles and the variation in allelic frequencies.(ABSTRACT TRUNCATED AT 250 WORDS)     

Genetic variation for preadult viability in Drosophila melanogaster

The extent of genetic variation in fitness and its components and genetic variation's dependence on environmental conditions remain key issues in evolutionary biology. We present measurements of genetic variation in preadult viability in a laboratory-adapted population of Drosophila melanogaster, made at four different densities. By crossing flies heterozygous for a wild-type chromosome and one of two different balancers (TM1, TM2), we measure both heterozygous (TM1/+, TM2/+) and homozygous (+/+) viability relative to a standard genotype (TM1/TM2). Forty wild-type chromosomes were tested, of which 10 were chosen to be homozygous viable. The mean numbers produced varied significantly between chromosome lines, with an estimated between-line variance in log(e) numbers of 0.013. Relative viabilities also varied significantly across chromosome lines, with a variance in log(e) homozygous viability of 1.76 and of log(e) heterozygous viability of 0.165. The between-line variance for numbers emerging increased with density, from 0.009 at lowest density to 0.079 at highest. The genetic variance in relative viability increases with density, but not significantly. Overall, the effects of different chromosomes on relative viability were remarkably consistent across densities and across the two heterozygous genotypes (TM1, TM2). The 10 lines that carried homozygous viable wild-type chromosomes produced significantly more adults than the 30 lethal lines at low density and significantly fewer adults at the highest density. Similarly, there was a positive correlation between heterozygous viability and mean numbers at low density, but a negative correlation at high density.     

Effects of genetic drift on variance components under a general model of epistasis

We analyze the changes in the mean and variance components of a quantitative trait caused by changes in allele frequencies, concentrating on the effects of genetic drift. We use a general representation of epistasis and dominance that allows an arbitrary relation between genotype and phenotype for any number of diallelic loci. We assume initial and final Hardy-Weinberg and linkage equilibrium in our analyses of drift-induced changes. Random drift generates transient linkage disequilibria that cause correlations between allele frequency fluctuations at different loci. However, we show that these have negligible effects, at least for interactions among small numbers of loci. Our analyses are based on diffusion approximations that summarize the effects of drift in terms of F, the inbreeding coefficient, interpreted as the expected proportional decrease in heterozygosity at each locus. For haploids, the variance of the trait mean after a population bottleneck is var(delta(z)) = sigma(n)k=1 FkV(A(k)), where n is the number of loci contributing to the trait variance, V(A(1)) = V(A) is the additive genetic variance, and V(A(k)) is the kth-order additive epistatic variance. The expected additive genetic variance after the bottleneck, denoted (V*(A)), is closely related to var(delta(z)); (V*(A)) = (1 - F) sigma(n)k=1 kFk-1V(A(k)). Thus, epistasis inflates the expected additive variance above V(A)(1 - F), the expectation under additivity. For haploids (and diploids without dominance), the expected value of every variance component is inflated by the existence of higher order interactions (e.g., third-order epistasis inflates (V*(AA. This is not true in general with diploidy, because dominance alone can reduce (V*(A)) below V(A)(1 - F) (e.g., when dominant alleles are rare). Without dominance, diploidy produces simple expressions: var(delta(z)) = sigma(n)k=1 (2F)kV(A(k)) and (V(A)) = (1 - F) sigma(n)k=1 k(2F)k-1V(A(k)). With dominance (and even without epistasis), var(delta(z)) and (V*(A)) no longer depend solely on the variance components in the base population. For small F, the expected additive variance simplifies to (V*(A)) approximately equal to (1 - F)V(A) + 4FV(AA) + 2FV(D) + 2FC(AD), where C(AD) is a sum of two terms describing covariances between additive effects and dominance and additive X dominance interactions. Whether population bottlenecks lead to expected increases in additive variance depends primarily on the ratio of nonadditive to additive genetic variance in the base population, but dominance precludes simple predictions based solely on variance components. We illustrate these results using a model in which genotypic values are drawn at random, allowing extreme and erratic epistatic interactions. Although our analyses clarify the conditions under which drift is expected to increase V(A), we question the evolutionary importance of such increases.     

The Genetic Structure of Natural Populations of DROSOPHILA MELANOGASTER. Xv. Nature of Developmental Homeostasis for Viability

Developmental homeostasis of relative viability was examined for homozygotes and heterozygotes using second chromosomes from two populations of Drosophila melanogaster. One was a chromosome population in which spontaneous mutations were allowed to accumulate since it was begun with a single near-normal second chromosome. The second was a natural population approximately at equilibrium. For the estimation of relative viability, the Cy method was employed (Wallace 1956), and environmental variance between simultaneously replicated cultures was used as the index of developmental homeostasis. A new method was used in the estimation of sampling variance for relative viability that was employed for the calculation of environmental variance (error variance between simultaneously replicated cultures - sampling variance). The following findings were obtained.: (1) The difference in environmental variance between homozygotes and heterozygotes could not be seen when a chromosome population with variation due to new mutations was tested. (2) When a chromosome group isolated from an approximate equilibrium population was examined, heterozygotes manifested a smaller environmental variance than the homozygotes if their relative viabilities were approximately the same. (3) There was a slight negative correlation between viability and environmental variance, although opposite results were found when the viabilities of individuals were high, especially when overdominance (coupling overdominance, Mukai 1969 a, b) was manifest. On the basis of these findings, it was concluded that developmental homeostasis was a product of natural selection, and its mechanism was discussed.     

Incipient Speciation by Sexual Isolation in Drosophila Melanogaster: Extensive Genetic Divergence without Reinforcement

The collection of Drosophila melanogaster from Zimbabwe and nearby regions (the Z-type) yield females who would not mate with the cosmopolitan D. melanogaster males (the M-type). To dissect the genetic basis of this sexual isolation, we constructed 16 whole-chromosome substitution lines between two standard Z-and M-lines. The results were as follows: (1) All substitution lines appear normal in viability and fertility in both sexes, indicating no strong postmating isolation. (2) The genes for the behaviors are mapped to all three major chromosomes with the same ranking and comparable magnitude of effects for both sexes: III > II >> X >/= 0 (III, II and X designate the effects of the three chromosomes). The results suggest less evolution on the X than on autosomes at loci of sexual behavior. (3) The genes for ``Z-maleness' are many and somewhat redundant. Whole-chromosome effects for Z-maleness appear nearly additive and show little dominance. (4) In contrast, ``Z-femaleness' has less redundancy as partial genotypes never exhibit full phenotypic effects. Epistatic interactions and incomplete dominance can sometimes be detected. (5) The extensive genetic divergence underlying sexual isolation has evolved in the absence of detectable reduction in hybrid fitnesses. Sexual selection has apparently been a driving force of multiple facets of speciation at the nascent stage without reinforcement.     

Quantitative genetic study on sexual difference in emigration behavior of Drosophila melanogaster in a natural population.

A quantitative genetic analysis was conducted on emigration response behavior using 140 second chromosome lines of Drosophila melanogaster. Fourteen sets of 5 x 5 partial diallel cross experiments were made in the parental generation. The emigration activity per batch of 50 male and 50 female F1 progeny was scored with Sakai's population system. Sexual difference did not appear in the emigration activity in these experiments. A significant genotype x sex x set interaction was detected. The genetic variance components of emigration activity differed between sexes: In males, additive genetic variance of emigration activity was 0.0497 +/- 0.0092 and dominance variance, 0.0018 +/- 0.0046; in females, additive, 0.0373 +/- 0.0076 and dominance, 0.0169 +/- 0.0044. Additive genetic correlation between sexes for the emigration activity was 0.685 +/- 0.150, deviating significantly from unity. These results suggested that the genes affecting emigration activity would operate differently between sexes of D. melanogaster in natural populations.     

Genetic aspects of aflatoxin B1 resistance in Drosophila melanogaster

Fifteen wild-type laboratory strains of Drosophila melanogaster were tested for egg-adult viability when exposed to larval development in media containing 0.5 and 1.0 ppm aflatoxin B (AFB1). Significant variation among the strains was demonstrated, especially at the 0.5 ppm AFB1 concentration. Two resistant and two sensitive strains were made isogenic and mated in a 4 X 4 diallel system. Results indicate that differences in AFB1 sensitivity are due to genes with additive effects on viability and that nonsystematic effects due to the interaction of cytoplasms and genes of both paternal and maternal origin are present. A chromosome/cytoplasm substitution analysis was performed using one of the sensitive and one of the resistant strains. Results indicate that genes on chromosomes X and 2 contribute to egg-adult viability differences observed for larval growth on media containing 0.5 and 1.0 ppm AFB1. Also, a significant interaction between chromosome 2 and cytoplasm, both from the resistant strain, was observed, resulting in a twofold increase in viability at 0.5 ppm AFB1 when compared to controls. Possible relationships of these findings with those from vertebrate systems are discussed.     

Genetic Analysis of Chromosomal Region 67a-D of Drosophila Melanogaster

In an effort to (1) characterize the 67 interval of chromosome 3 of Drosophila melanogaster genetically and (2) isolate mutations of the 67B1 small heat shock protein (hsp) gene cluster specifically, we undertook a mutational analysis of the 67A-D subinterval. Using a deficiency of the 67A2 to 67D11-13 region, Df(3L)AC1, we screened 8700 diepoxybutane-treated chromosomes and 7800 ethyl methanesulfonate-treated chromosomes for visible and lethal mutations throughout this interval and recovered 74 independent recessive lethal mutations, but no visible mutations. One of the lethal mutations, d29A6, was identified as an overlapping deficiency extending from 66F3 to 67B1. An additional 6000 diepoxybutane-treated chromosomes were screened for lethality over d29A6, yielding another four lethal mutations within the 67A2-B1 subinterval. These 78 lethal mutations, along with two others isolated in other laboratories, define 23 essential loci--6 within the 67A2-B1 subinterval and 17 within the 67A2 to D11-13 subinterval. Many of these loci appear to be required for imaginal development only, exhibiting late larval to pharate adult lethal phases. Examination of the 67A2-B1 lethal complementation groups for (1) earlier onset of lethality following a heat shock, (2) missing or altered small hsps on two-dimensional protein gels, and (3) restoration of viability by transformed wild-type copies of the small hsp genes indicates that none of these mutations affect the small hsps. On the basis of this analysis and the known homology of the genes, we conclude that the small hsps are functionally equivalent.     

The Genetic Structure of Natural Populations of DROSOPHILA MELANOGASTER. Xii. Linkage Disequilibrium in a Large Local Population

Seven hundred and three second chromosomes were extracted from a Raleigh, North Carolina population of Drosophila melanogaster in 1970. Additionally, four hundred and eighty-nine third chromosomes were extracted from a large cage population founded from the flies in the 1970 Raleigh collection. The alpha glycerol-3-phosphate dehydrogenase-1, malate dehydrogenase-1, alcohol dehydrogenase, and alpha amylase loci were studied from the second chromosomes, and the esterase-6, esterase-C, and octanol dehydrogenase loci were analyzed from the third chromosomes. Inversions, relative viability and fecundity were studied for both classes of chromosomes. The following significant findings were obtained: (1) All loci examined were polymorphic or had at least two alleles at appreciable frequencies. Analysis of the combined data from this experiment with that of Mukai, Mettler and Chigusa (1971) revealed that the frequencies of the genes in the second chromosomes collected in early August were approximately the same over three years. (2) Linkage disequilibria between and among isozyme genes inter se were not detected except in a few cases which can be considered due to non-random sampling. (3) Linkage disequilibria between isozyme genes and polymorphic inversions were detected when the recombination values between the breakage points of the inversions and the genes in question were small. In only a few cases, were second and third order linkage disequilibria including polymorphic inversions detected. (4) Evidence for either variation among genotypes within loci or cumulative effects of heterozygosity was found for viability and fecundity. As a result of these findings, it was tentatively concluded that although selection might be perceptibly operating on some polymorphic isozyme loci, most of the polymorphic isozyme genes are selectively neutral or near-neutral in the populations studied.     

Genetic study on emigration behavior of Drosophila melanogaster in a natural population

Genetic study on emigration behavior of Drosophila melanogaster in the Ishinomaki population was conducted with 140 2nd chromosome lines. Fourteen sets of 5X5 partial diallel cross experiments were made to examine the emigration activity of F1 progeny. Emigration activity was scored using the method of Sakai et al. (1958). Additive genetic variance was 0.0377 +/- 0.0069 and dominance variance 0.0076 +/- 0.0032. The average degree of dominance of mildly deleterious genes for emigration activity in an equilibrium population was 0.069 +/- 0.042. The estimated degree of dominance at a gene locus affecting emigration activity was 0.067, which revealed nearly complete dominance for the tendency of heterozygote flies to move from their original place to another. Average degree of dominance of lethal gene for emigration activity was 0.012.