Effects of different base populations on selection response in Drosophila

Oregon‐R, +3, and crossbred strains of Drosophila melanogaster were tested for their response to selection for abdominal bristle number. Various subsidiary tests, consisting of heritability estimations, testing for lethal second and third chromosomes, and chromosome assays were conducted on the selection replicates, which had undergone 14 generations of selection. Evidence showed that a plateau which occurred very early in the +3 high selection replicates was due to fixation of a few additive genes with large effects, thus accounting for the low phenotypic and additive genetic variance, the slight regression in abdominal bristle number on relaxation of selection, the absence of directional dominance, and the low frequency of recessive lethals.

High frequencies of second and third chromosome lethals were found in the Oregon‐R high and low replicates and in the +3 low replicates. That these lethals were not selected for heterozygote superiority for extreme bristle effect was indicated by the slight regression of these replicates on relaxation of selection, and by the absence of high, fluctuating phenotypic variances.

From chromosome assays it appears that the two parental strains had different arrays of genes affecting high bristle number, with these genes located mostly in chromosome II in the Oregon‐R high line but in chromosome III in the +3 high line. In the Crossbred high line, high bristle factors were located in both the second and third chromosomes. The low bristle factors were located mainly in the second chromosome in all three low selection lines.

It appears that the original cross had combined different genes favouring high bristle number, thus allowing greater response in the Crossbred high selection line. The same did not occur for low selection; the response from the Crossbred low line was similar to that of the parental low lines, suggesting that the gene arrays affecting low bristle number in the two original populations were comparable.     

High Rates of Occurrence of Spontaneous Chromosome Aberrations in DROSOPHILA MELANOGASTER

Spontaneous mutations were accumulated for 40 generations in 140 unrelated second chromosomes with the standard gene arrangement. These were extracted from the same population by using the marked inversion technique, and the following findings were obtained: (1) In 42 out of the 140 chromosome lines, chromosome aberrations were detected by examining the salivary gland chromosomes: 40 paracentric and 15 pericentric inversions, 2 reciprocal translocations between the second and the third chromosomes, and 6 transpositions. (2) In 63 out of the 90 originally lethal-free lines, recessive lethal mutations occurred. (3) There were only 3 lines that acquired chromosome aberrations (inversions) with no lethal effects in the homozygous condition. (4) In a comparison of these results with those of the (CH), (PQ), and (RT) chromosomes in which no chromosome aberrations occurred after accumulating mutations for 22058 chromosome.generations (Yamaguchi and Mukai 1974), it was concluded that some of these 140 chromosomes carried a kind of mutator. (5) The frequency of mutator-carrying chromosome lines was estimated to be 0.66 on the basis of the distribution of the break-points on the chromosome lines and the frequency of lines that acquired neither recessive lethal mutations nor chromosome aberrations. Thus, the average number of breaks per mutator-carrying chromosome was estimated to be about 0.19/generation.On the basis of these estimates, the nature of the mutator factor was discussed.     

Mutation Rate and Dominance of Genes Affecting Viability in DROSOPHILA MELANOGASTER

Spontaneous mutations were allowed to accumulate in a second chromosome that was transmitted only through heterozygous males for 40 generations. At 10-generation intervals the chromosomes were assayed for homozygous effects of the accumulated mutants. From the regression of homozygous viability on the number of generations of mutant accumulation and from the increase in genetic variance between replicate chromosomes it is possible to estimate the mutation rate and average effect of the individual mutants. Lethal mutations arose at a rate of 0.0060 per chromosome per generation. The mutants having small effects on viability are estimated to arise with a frequency at least 10 times as high as lethals, more likely 20 times as high, and possibly many more times as high if there is a large class of very nearly neutral mutations.-The dominance of such mutants was measured for chromosomes extracted from a natural population. This was determined from the regression of heterozygous viability on that of the sum of the two constituent homozygotes. The average dominance for minor viability genes in an equilibrium population was estimated to be 0.21. This is lower than the value for new mutants, as expected since those with the greatest heterozygous effect are most quickly eliminated from the population. That these mutants have a disproportionately large heterozygous effect on total fitness (as well as on the viability component thereof) is shown by the low ratio of the genetic load in equilibrium homozygotes to that of new mutant homozygotes.     

Genetic consequences of linkage between malathion resistance and an autosomal male-determining factor in house fly (Diptera: Muscidae).

The pattern of inheritance of genes conferring resistance to malathion and genetic consequences of linkage between an autosomal male-determining factor and resistance genes on the second chromosome were investigated in a strain of house fly, Musca domestica L., selected for malathion resistance. The second and fifth chromosomes contribute significantly to malathion resistance. The presence of a male-determining factor linked with the resistance genes on the second chromosome resulted in a strong sexual dimorphism in malathion resistance. We also observed that the male-determining factor changed its linkage relationship from the third linkage group to the second linkage group during the selection experiments.     

Genetic basis of cross-resistance to three organophosphate insecticides in Drosophila melanogaster (Diptera: Drosophilidae)

To investigate the genetic basis of cross-resistance to insecticides, we conducted genetic analyses of resistance to three organophosphate insecticides, malathion, prothiophos, and fenitrothion. After isofemale lines resistant and susceptible to all of the three organophosphates had been screened from natural populations of Drosophila melanogaster (Meigen), chromosomal analyses were performed by using chromosome-substituted lines between the resistant and the susceptible lines. The chromosomal analyses revealed that both the second and the third chromosomes contributed to resistance to the organophosphates, suggesting that this resistant line possessed at least two factors for organophosphate resistance. However, the relative contribution of each chromosome was different in resistance to different organophosphates. We further carried out genetic mapping of a resistance factor for each organophosphate on each of the two chromosomes. Each resistance factor was mapped to the position of each chromosome, about II-62 and III-50. Results of the chromosomal analyses and the genetic mapping revealed that at least two resistance factors exhibiting different patterns of cross-resistance to the organophosphates existed within a natural population of D. melanogaster. Based on this research, genetic variation in insecticide resistance within natural populations and complex as well as simple aspects of the mechanism of cross-resistance are discussed.     

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.     

Quantitative trait loci for thermotolerance phenotypes in Drosophila melanogaster

For insects, temperature is a major environmental variable that can influence an individual's behavioral activities and fitness. Drosophila melanogaster is a cosmopolitan species that has had great success in adapting to and colonizing diverse thermal niches. This adaptation and colonization has resulted in complex patterns of genetic variation in thermotolerance phenotypes in nature. Although extensive work has been conducted documenting patterns of genetic variation, substantially less is known about the genomic regions or genes that underlie this ecologically and evolutionarily important genetic variation. To begin to understand and identify the genes controlling thermotolerance phenotypes, we have used a mapping population of recombinant inbred (RI) lines to map quantitative trait loci (QTL) that affect variation in both heat- and cold-stress resistance. The mapping population was derived from a cross between two lines of D. melanogaster (Oregon-R and 2b) that were not selected for thermotolerance phenotypes, but exhibit significant genetic divergence for both phenotypes. Using a design in which each RI line was backcrossed to both parental lines, we mapped seven QTL affecting thermotolerance on the second and third chromosomes. Three of the QTL influence cold-stress resistance and four affect heat-stress resistance. Most of the QTL were trait or sex specific, suggesting that overlapping but generally unique genetic architectures underlie resistance to low- and high-temperature extremes. Each QTL explained between 5 and 14% of the genetic variance among lines, and degrees of dominance ranged from completely additive to partial dominance. Potential thermotolerance candidate loci contained within our QTL regions are identified and discussed.     

Effects of marker chromosomes on relative viability

Viability relative to Cy/Pm as a standard was studied in Drosophila melanogaster. One experiment, E1, consisted of progeny from eleven distinct 7 x 7 factorial mating designs with reciprocals for second chromosomes extracted from a natural population. The other experiment, E2, consisted of two distinct sets of heterozygotes with reciprocals and corresponding homozygotes. It was established from E1 that there are little to no synergistic effects among different genotypes in a vial and that Cy and Pm heterozygotes vary almost as much as would be expected if one chromosome were held constant for wild-type heterozygotes. In wild-type heterozygotes, variances were estimated to be 0.0099 for average chromosomal effects, 0.0054 for interactions of chromosomes, 0.0021 for maternal effects, 0.0079 for paternal effects, and -0.0010 for the remaining interaction effects, all being significantly different from zero except the last. The variances of Cy and Pm heterozygotes, covariance of Cy and Pm heterozygotes, and covariances of Cy and Pm heterozygotes with wild-type heterozygotes, as well as the comparable statistics available in E2, all showed a large paternal component of variance and a smaller maternal component of variance, both unexpected results.—From E2 the variance of homozygotes, excluding error variance, was estimated to be 0.0149, and the covariances of homozygotes with wild-type heterozygotes to be 0.0056 for maternally derived chromosomes common and 0.0126 for paternally derived chromosomes common, again showing the larger paternal than maternal influence. The average genetic regression of heterozygotes on homozygotes of 0.61 was reduced only slightly to 0.56 by correcting for maternal and paternal variances. These genetic regressions, generally utilized as estimators of the average degree of dominance, are larger than any previously reported.—Differential meiotic drive in Cy and Pm parents was shown to be compatible with the large paternal and maternal variances, but other causes cannot be ruled out.—Approximations were developed for translating various variances, covariances, and regressions between single- and double-marker experiments, assuming that marker chromosomes behave as typical wild-type chromosomes in one case and assuming a (partially) recessive model with the population in mutation selection balance in another case. Various features, particularly the estimation of dominance, were compared and discussed between the two cases.     

The comparison of intrinsic rates of increase among chromosome-substituted lines resistant and susceptible to organophosphate insecticides in Drosophila melanogaster

To investigate the genetic basis of the seasonal fluctuations in resistance to three organophosphates, observed within a natural population of Drosophila melanogaster (Meigen), we compared the intrinsic rate of increase, generation time and net reproduction rate among chromosome substitution lines derived from a resistant and a susceptible line, obtained from this natural population. There was significant variation among substituted lines; lines possessing the third chromosome from the resistant line, which confers resistance to the three organophosphates, generally showed lower mean values of these fitness measures. Chromosomal analyses also indicated significant negative contributions of the third chromosome from the resistant line. However, significant positive contributions of the interactions among chromosomes from the resistant line to these fitness measures were also detected. We further conducted a local stability analysis, in which each chromosome-substituted line was assumed to be introduced at a low frequency into the initial susceptible population. It was demonstrated that the resistance factor(s) on the third chromosome tend to decrease in their frequency under both density-independent and juvenile density-regulated conditions. Based on these results, a possible explanation for the seasonal fluctuations in resistance to the three organophosphates observed in the natural population was proposed.     

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.     

Viabilities of Third Chromosomes of DROSOPHILA PSEUDOOBSCURA Differing in Relative Competitive Fitness

Arrowhead (AR) third chromosome arrangements of Drosophila pseudoobscura, whose competitive fitnesses had been determined in population cages, were tested for their genetic loads in homozygous, heterozygous (homokaryotypic), and heterokaryotypic (AR/CH) combinations. The results showed that their competitive population cage performances were correlated to their viabilities as homozygotes but were not correlated to their viabilities as heterozygotes or as heterokaryotypes. However, the results do not fit in too simply with the mutational model of population structure, since the improvement of homozygous viability with increased competitive fitness was not accompanied by a significant degree of dominance as measured by the regression of viabilities of heterozygotes on homozygotes. Only the AR chromosomes derived from the population with poorest competitive fitness showed marked partial dominance (h=.35). The viabilities of heterokaryotypes were markedly uniform for all chromosomes tested and produced significantly greater numbers of flies per culture than the homokaryotypes. In general, the results show that the ranking of relative competitive fitnesses of these chromosomes is not a simple extrapolation of their viabilities, although marked changes in the populations tested have occurred. It is proposed that the differences in competitive fitness, homozygous viability, and degree of dominance observed among these chromosomes, arise from differences in genetic variability which enable different linkage relationships to be established for genes affecting these attributes.     

Adaptive protein evolution of X-linked and autosomal genes in Drosophila: implications for faster-X hypotheses

Patterns of sex chromosome and autosome evolution can be used to elucidate the underlying genetic basis of adaptative change. Evolutionary theory predicts that X-linked genes will adapt more rapidly than autosomes if adaptation is limited by the availability of beneficial mutations and if such mutations are recessive. In Drosophila, rates of molecular divergence between species appear to be equivalent between autosomes and the X chromosome. However, molecular divergence contrasts are difficult to interpret because they reflect a composite of adaptive and nonadaptive substitutions between species. Predictions based on faster-X theory also assume that selection is equally effective on the X and autosomes; this might not be true because the effective population sizes of X-linked and autosomal genes systematically differ. Here, population genetic and divergence data from Drosophila melanogaster, Drosophila simulans, and Drosophila yakuba are used to estimate the proportion of adaptive amino acid substitutions occurring in the D. melanogaster lineage. After gene composition and effective population size differences between chromosomes are controlled, X-linked and autosomal genes are shown to have equivalent rates of adaptive divergence with approximately 30% of amino acid substitutions driven by positive selection. The results suggest that adaptation is either unconstrained by a lack of beneficial genetic variation or that beneficial mutations are not recessive and are thus highly visible to natural selection whether on sex chromosomes or on autosomes.     

Genetic variation for total fitness in Drosophila melanogaster: complex yet replicable patterns

The extent of genetic variation in fitness is a crucial issue in evolutionary biology and yet remains largely unresolved. In Drosophila melanogaster, we have devised a method that allows the net effects on fitness of heterozygous wild-type chromosomes to be measured, by competing them against two different "balancer" chromosomes. We have applied the method to a large sample of 40 wild-type third chromosomes and have measured fitnesses of nonlethal chromosomes as well as chromosomes bearing recessive lethals. The measurements were made in the environment to which the population was adapted and did not involve inbreeding. The results show an extraordinary similarity in the behavior of replicates of the same chromosome, indicating consistent genetic effects on total fitness. Some invading chromosomes increased rapidly and some slowly, and some rose to appreciable frequency after several months, but then declined again: in every case, the same pattern was seen in each replicate. We estimated relative fitnesses, rates of change of fitness, and relative viabilities, for each chromosome. There were significant fluctuations around the fitted model, which were also highly replicable. Wild-type chromosomes varied substantially in their effects on heterozygous fitness, and these effects vary through time, most likely as a result of genotype x environment interactions.     

The Genetic Structure of Natural Populations of Drosophila Melanogaster. Xxiv. Effects of Hybrid Dysgenesis on the Components of Genetic Variance of Viability

Eight hundred second chromosomes were extracted from the Ishigakijima population, one of the southernmost populations of Drosophila melanogaster in Japan. Half of them were extracted in Native cytoplasm (P-type), and half in Foreign cytoplasm (M-type). Various population-genetic parameters, including the frequency of lethal-carrying second chromosomes (Q = 0.235 for the Native; 0.218 for the Foreign), the allelism rate of lethal second chromosome (Ic = 0.0217 for the Native; 0.0134 for the Foreign), the homozygous detrimental and lethal loads (D = 0.179 for the Native; 0.270 for the Foreign; L = 0.262 for the Native; 0.240 for the Foreign), the average degree of dominance of mildly deleterious mutations (?E = 0.244 for the Native; 0.208 for the Foreign), and the components of genetic variance for viability [additive (sigma A2) and dominance (sigma D2)](?igma A2 = 0.0187 for the Native; 0.0172 for the Foreign; ?igma D2 = 0.0005 for the Native; 0.0009 for the Foreign) were estimated. The data indicate that D was significantly larger and hE was significantly smaller in the Foreign cytoplasm. However, the estimates of additive and dominance variances were not significantly different between the two cytoplasms. The additive genetic variance for viability in the Ishigakijima population was greater than expected on the basis of mutation-selection balance confirming previous studies on papers of D. melanogaster in warm climates.     

Signals of demographic expansion in Drosophila virilis

Background

The antagonistic co-evolution of hosts and their parasites is considered to be a potential driving force in maintaining host genetic variation including sexual reproduction and recombination. The examination of this hypothesis calls for information about the genetic basis of host-parasite interactions – such as how many genes are involved, how big an effect these genes have and whether there is epistasis between loci. We here examine the genetic architecture of quantitative resistance in animal and plant hosts by concatenating published studies that have identified quantitative trait loci (QTL) for host resistance in animals and plants.

Results

Collectively, these studies show that host resistance is affected by few loci. We particularly show that additional epistatic interactions, especially between loci on different chromosomes, explain a majority of the effects. Furthermore, we find that when experiments are repeated using different host or parasite genotypes under otherwise identical conditions, the underlying genetic architecture of host resistance can vary dramatically – that is, involves different QTLs and epistatic interactions. QTLs and epistatic loci vary much less when host and parasite types remain the same but experiments are repeated in different environments.

Conclusion

This pattern of variability of the genetic architecture is predicted by strong interactions between genotypes and corroborates the prevalence of varying host-parasite combinations over varying environmental conditions. Moreover, epistasis is a major determinant of phenotypic variance for host resistance. Because epistasis seems to occur predominantly between, rather than within, chromosomes, segregation and chromosome number rather than recombination via cross-over should be the major elements affecting adaptive change in host resistance.     

Genetic dissection of chromosome substitution lines of cotton to discover novel Gossypium barbadense L. alleles for improvement of agronomic traits

We recently released a set of 17 chromosome substitution (CS-B) lines (2n = 52) that contain Gossypium barbadense L. doubled-haploid line ‘3-79’ germplasm systematically introgressed into the Upland inbred ‘TM-1’ of G. hirsutum (L.). TM-1 yields much more than 3-79, but cotton from the latter has superior fiber properties. To explore the use of these quasi-isogenic lines in studying gene interactions, we created a partial diallel among six CS-B lines and the inbred TM-1, and characterized their descendents for lint percentage, boll weight, seedcotton yield and lint yield across four environments. Phenotypic data on the traits were analyzed according to the ADAA genetic model to detect significant additive, dominance, and additive-by-additive epistasis effects at the chromosome and chromosome-by-chromosome levels of CS-B lines. For example, line 3-79 had the lowest boll weight, seedcotton yield and lint yield, but CS-B22Lo homozygous dominance genetic effects on seedcotton and lint yield were nearly four times those of TM-1, and its hybrids with TM-1 had the highest additive-by-additive epistatic effects on seedcotton and lint yield. CS-B14sh, 17, 22Lo and 25 produced positive homozygous dominance effects on lint yield, whereas doubly heterozygous combinations of CS-B14sh with CS-B17, 22Lo and 25 produced negative dominance effects, suggesting that epistatic effects between genes in these chromosomes strongly affect lint yield. The results underscore the opportunities to systematically identify genomic regions harboring genes that impart agronomically significant effects via epistatic interactions. The chromosome-by-chromosome approach significantly complements other strategies to detect and quantify epistatic interaction effects, and the quasi-isogenic nature of families and lines from CS-B intermatings will facilitate high-resolution localization, development of markers for selection and map-assisted identification of genes involved in strong epistatic effects.     

Genetic effects of individual chromosomes in cotton cultivars detected by using chromosome substitution lines as genetic probes

Determination of chromosomes or chromosome arms with desirable genes in different inbred lines and/or crosses should provide useful genetic information for crop improvement. In this study, we applied a modified additive-dominance model to analyze a data set of 13 cotton chromosome substitution lines and their recurrent parent TM-1, five commercial cultivars, and their 70 F(2) hybrids. The chromosome additive and dominance variance components for eight agronomic and fiber traits were determined. On average, each chromosome or chromosome arm was associated with 6.5 traits in terms of additive and/or dominance effects. The chromosomes or chromosome arms, which contributed significant additive variances for the traits investigated, included 2, 16, 18, 25, 5sh (short arm), 14sh, 15sh, 22sh, and 22Lo (long arm). Chromosome additive effects were also predicted in this study. The results showed that CS-B 25 was favorably associated with several fiber traits, while FM966 was favorably associated with both yield and fiber traits with alleles on multiple chromosomes or chromosome arms. Thus, this study should provide valuable genetic information on pure line development for several improved traits such as yield and fiber quality.     

Chromosome Interactions in DROSOPHILA MELANOGASTER. II. Total Fitness

In a large experiment, using nearly 200 population cages, we have measured the fitness of Drosophila melanogaster homozygous (1) for the second chromosome, (2) for the third chromosome, and (3) for both chromosomes. Twentyfour second chromosomes and 24 third chromosomes sampled from a natural population were tested. The mean fitness of the homozygous flies is 0.081 ± 0.014 for the second chromosome, 0.080 ± 0.017 for the third chromosome, and 0.079 ± 0.024 for both chromosomes simultaneously. Assuming that fitnesses are multiplicative (the additive fitness model makes no sense in the present case because of the large selection coefficients involved), the expected mean fitness of the homozygotes for both chromosomes is 0.0066; their observed fitness is more than ten times greater. Thus, it appears that synergistic interactions between loci are considerable; and that, consequently, the fitness function substantially departs from linearity. Two models are tentatively suggested for the fitness function: a "threshold" model and a "synergistic" model.—The experiments reported here confirm previous results showing that the concealed genetic load present in natural populations of Drosophila is sufficient to account for the selective maintenance of numerous polymorphisms (of the order of 1000).     

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.     

An Integrated Genetic Map of the African Human Malaria Vector Mosquito, Anopheles Gambiae

We present a genetic map based on microsatellite polymorphisms for the African human malaria vector, Anopheles gambiae. Polymorphisms in laboratory strains were detected for 89% of the tested microsatellite markers. Genotyping was performed for individual mosquitoes from 13 backcross families that included 679 progeny. Three linkage groups were identified, corresponding to the three chromosomes. We added 22 new markers to the existing X chromosome map, for a total of 46 microsatellite markers spanning a distance of 48.9 cM. The second chromosome has 57 and the third 28 microsatellite markers spanning a distance of 72.4 and 93.7 cM, respectively. The overall average distance between markers is 1.6 cM (or 1.1, 1.2, and 3.2 cM for the X, second, and third chromosomes, respectively). In addition to the 131 microsatellite markers, the current map also includes a biochemical selectable marker, Dieldrin resistance (Dl), on the second chromosome and five visible markers, pink-eye (p) and white (w) on the X, collarless (c) and lunate (lu) on the second, and red-eye (r) on the third. The cytogenetic locations on the nurse cell polytene chromosomes have been determined for 47 markers, making this map an integrated tool for cytogenetic, genetic, and molecular analysis.