P element transposon-induced quantitative genetic variation for inebriation time in Drosophila melanogaster

1991 ◽  
Vol 81 (3) ◽  
pp. 317-320 ◽  
Author(s):  
R. Frankham ◽  
A. Torkamanzehi ◽  
C. Moran
Genetics ◽  
1998 ◽  
Vol 148 (4) ◽  
pp. 1885-1891 ◽  
Author(s):  
Grażyna M Fedorowicz ◽  
James D Fry ◽  
Robert R H Anholt ◽  
Trudy F C Mackay

Abstract Odor-guided behavior is a polygenic trait determined by the concerted expression of multiple loci. Previously, P-element mutagenesis was used to identify single P[lArB] insertions, in a common isogenic background, with homozygous effects on olfactory behavior. Here, we have crossed 12 lines with these smell impaired (smi) mutations in a half-diallel design (excluding homozygous parental genotypes and reciprocal crosses) to produce all possible 66 doubly heterozygous hybrids with P[lArB] insertions at two distinct locations. The olfactory behavior of the transheterozygous progeny was measured using an assay that quantified the avoidance response to the repellent odorant benzaldehyde. There was significant variation in general combining abilities of avoidance scores among the smi mutants, indicating variation in heterozygous effects. Further, there was significant variation among specific combining abilities of each cross, indicating dependencies of heterozygous effects on the smi locus genotypes, i.e., epistasis. Significant epistatic interactions were identified for nine transheterozygote genotypes, involving 10 of the 12 smi loci. Eight of these loci form an interacting ensemble of genes that modulate expression of the behavioral phenotype. These observations illustrate the power of quantitative genetic analyses to detect subtle phenotypic effects and point to an extensive network of epistatic interactions among genes in the olfactory subgenome.


1980 ◽  
Vol 77 (2) ◽  
pp. 1073-1077 ◽  
Author(s):  
C. C. Laurie-Ahlberg ◽  
G. Maroni ◽  
G. C. Bewley ◽  
J. C. Lucchesi ◽  
B. S. Weir

Genetics ◽  
1985 ◽  
Vol 111 (2) ◽  
pp. 351-374
Author(s):  
Trudy F C Mackay

ABSTRACT The P family of transposable elements in Drosophila melanogaster transpose with exceptionally high frequency when males from P strains carrying multiple copies of these elements are crossed to females from M strains that lack P elements, but with substantially lower frequency in the reciprocal cross. Transposition is associated with enhanced mutation rates, caused by insertion and deletion of P elements, and chromosome rearrangements. If P element mutagenesis creates additional variation for quantitative traits, accelerated response to artificial selection of progeny of M♀♀ × P♂♂ strain crosses is expected, compared with that from progeny of P♀♀ × M♂♂ strain crosses.—Divergent artificial selection for number of bristles on the last abdominal tergite was carried out for 16 generations among the progeny of P–strain males (Harwich) and M–strain females (Canton-S) and also of M–strain males (Canton-S) and P-strain females (Harwich). Each cross was replicated four times. Average realized heritability of abdominal bristle score for the crosses in which P transposition was expected was 0.244 ± 0.017, 1.5 times greater than average heritability estimated from crosses in which transposition was expected to be rare (0.163 ± 0.010). Phenotypic variance of abdominal bristle score increased by a factor of four in lines selected from M♀♀ × P♂♂ crosses when compared with those selected from P♀♀ × M♂♂ hybrids. Not all quantitative genetic variation induced by P elements is additive. A substantial fraction of nonadditive genetic variation is implicated by chromosomal analysis, which demonstrates deleterious fitness effects of the mutations when homozygous.—Several putative "quantitative" mutations were identified from chromosomes extracted from the selected lines; these will form the basis for further investigation at the molecular level of the genes controlling quantitative inheritance.


2005 ◽  
Vol 85 (1) ◽  
pp. 47-55 ◽  
Author(s):  
DEAN M. GILLIGAN ◽  
DAVID A. BRISCOE ◽  
RICHARD FRANKHAM

Quantitative genetic variation, the main determinant of the ability to evolve, is expected to be lost in small populations, but there are limited data on the effect, and controversy as to whether it is similar to that for near neutral molecular variation. Genetic variation for abdominal and sternopleural bristle numbers and allozyme heterozygosity were estimated in 23 populations of Drosophila melanogaster maintained at effective population sizes of 25, 50, 100, 250 or 500 for 50 generations, as well as in 19 highly inbred populations and the wild outbred base population. Highly significant negative regressions of proportion of initial genetic variation retained on inbreeding due to finite population size were observed for both quantitative characters (b=−0·67±0·14 and −0·58±0·11) and allozyme heterozygosity (b=−0·79±0·10), and the regression coefficients did not differ significantly. Thus, quantitative genetic variation is being lost at a similar rate to molecular genetic variation. However, genetic variation for all traits was lost at rates significantly slower than predicted by neutral theory, most likely due to associative overdominance. Positive, but relatively low correlations were found among the different measures of genetic variation, but their low magnitudes were attributed to large sampling errors, rather than differences in the underlying processes of loss.


2018 ◽  
Author(s):  
Enoch Ng’oma ◽  
Wilton Fidelis ◽  
Kevin M. Middleton ◽  
Elizabeth G. King

AbstractThe nutritional conditions experienced by a population play a major role in shaping trait evolution in many taxa. Constraints exerted by nutrient limitation or nutrient imbalance can influence the maximal value that fitness components such as reproduction and lifespan attains, and organisms may shift how resources are allocated to different structures and functions in response to changes in nutrition. Whether the phenotypic changes associated with changes in nutrition represent an adaptive response is largely unknown. Further, it is unclear whether the response of fitness components to diet even has the potential to evolve in most systems. In this study, we use an admixed multiparental population of Drosophila melanogaster reared in three different diet conditions to estimate quantitative genetic parameters for lifespan and fecundity. We find significant genetic variation for both traits in our population and show that lifespan has moderate to high heritabilities within diets. Genetic correlations for lifespan between diets were significantly less than one, demonstrating a strong genotype by diet interaction. These findings demonstrate substantial standing genetic variation in our population that is comparable to natural populations and highlights the potential for adaptation to changing nutritional environments.


Author(s):  
Bruce Walsh ◽  
Michael Lynch

One of the major unresolved issues in quantitative genetics is what accounts for the amount of standing genetic variation in traits. A wide range of models, all reviewed in this chapter, have been proposed, but none fit the data, either giving too much variation or too little apparent stabilizing selection.


Genetics ◽  
1980 ◽  
Vol 95 (3) ◽  
pp. 727-742 ◽  
Author(s):  
R Frankham ◽  
D A Briscoe ◽  
R K Nurthen

ABSTRACT Abdominal bristle selection lines (three high and three low) and controls were founded from a marked homozygous line to measure the contribution of sex-linked "mutations" to selection response. Two of the low lines exhibited a period of rapid response to selection in females, but not in males. There were corresponding changes in female variance, in heritabilities in females, in the sex ratio (a deficiency of females) and in fitness, as well as the appearance of a mutant phenotype in females of one line. All of these changes were due to bb alleles (partial deficiencies for the rRNA tandon) in the X chromosomes of these lines, while the Y chromosomes remained wild-type bb+. We argue that the bb alleles arose by unequal crossing over in the rRNA tandon.—A prediction of this hypothesis is that further changes can occur in the rRNA tandon as selection is continued. This has now been shown to occur.—Our minimum estimate of the rate of occurrence of changes at the rRNA tandon is 3 × 10-4. As this is substantially higher than conventional mutation rates, the questions of the mechanisms and rates of origin of new quantitative genetic variation require careful re-examination.


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