Premium
THE RATE AND EFFECTS DISTRIBUTION OF VIABILITY MUTATION IN DROSOPHILA : MINIMUM DISTANCE ESTIMATION
Author(s) -
GarcíaDorado Aurora
Publication year - 1997
Publication title -
evolution
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.84
H-Index - 199
eISSN - 1558-5646
pISSN - 0014-3820
DOI - 10.1111/j.1558-5646.1997.tb03960.x
Subject(s) - biology , kurtosis , mutation , genetics , statistics , gene , mathematics
The empirical distribution of the mean viability of mutation accumulation lines, obtained from three published experiments, was analyzed using minimum‐distance estimation. In two cases (Mukai et al. 1972; Ohnishi 1977), mutations were allowed to accumulate in copies of chromosome II protected from natural selection and recombination. In the other one (Fernández and López‐Fanjul 1996), they accumulated in inbred lines derived from an isogenic stock. In contrast with currently accepted hypotheses, we consistently estimated low (about 0.01) genomic viability mutation rates, λ, and a small kurtosis of the distribution of mutational effects on viability ( a ) in the three datasets. Minimum‐distance estimates of the per‐generation mean viability change due to mutation (λ E [ a ]) were also obtained. These were very similar for both chromosomal datasets, their absolute values being about five times smaller than estimates obtained from the observed change in mean viability during the mutation process. It must be noted that, in both experiments, viability was measured relative to the Cy chromosome of a Cy/Pm stock. Thus, an unnoticed viability increase in this Cy chromosome may have resulted in overestimation of the mean viability reduction in the lines. In parallel, minimum‐distance estimation of λ E ( a ) from inbred lines data (where the selective pressure during the accumulation process was larger) was even somewhat smaller, in absolute value, and very close to the estimate obtained by comparing the mean viability of the lines with that of the control isogenic line. The evolutionary importance of these results, as well as their relevance to the solution of the mutational load paradox, is discussed.