THE MUTATION-RATE AND THE DISTRIBUTION OF MUTATIONAL EFFECTS OF VIABILITY AND FITNESS IN DROSOPHILA-MELANOGASTER

Citation
A. Garciadorado et al., THE MUTATION-RATE AND THE DISTRIBUTION OF MUTATIONAL EFFECTS OF VIABILITY AND FITNESS IN DROSOPHILA-MELANOGASTER, Genetica, 103, 1998, pp. 255-265
Citations number
29
Categorie Soggetti
Genetics & Heredity
Journal title
ISSN journal
00166707
Volume
103
Year of publication
1998
Pages
255 - 265
Database
ISI
SICI code
0016-6707(1998)103:<255:TMATDO>2.0.ZU;2-A
Abstract
The empirical distributions of the average viability and fitness of mu tation accumulation lines of Drosophila melanogaster were analyzed usi ng minimum distance estimation. Data come from two different experimen tal designs where mutations were allowed to accumulate: 1) in copies o f chromosome II protected from natural selection and recombination (vi ability: Mukai et al., 1972; Ohnishi, 1977; fitness: Houle et al., 199 2), 2) in inbred lines derived from the same isogenic stock (viability : Fernandez & Lopez-Fanjul, 1996; fitness: this paper). Information fr om all data sets converged, indicating that the mutational rates were small, about 1% for viability and 3% for fitness. For both traits, the rate of mutational decline appears to be smaller than suggested by pr evious studies (about one-fifth of the latter), the average mutational effect was neither severe nor very slight, ranging from -0.1 to -0.3, and the distribution of mutant effects was, at most, slightly leptoku rtic. Therefore, the mutational load in natural populations is one to two orders of magnitude smaller than previously thought las based upon analyses conditional to estimates of the mutational decline of viabil ity or fitness that appear to be biased upward). Over 95% of the mutat ional variance of each trait was contributed by non-slightly deleterio us mutations (absolute homozygous effect larger than 0.03 or 0.1, depe nding on the data set considered) occurring at a rate not higher than 0.025 per haploid genome and generation. Our data suggest that most de leterious mutations affecting fitness act mainly through a single comp onent-trait.