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Transposable element-induced fitness mutations in Drosophila melanogaster

Published online by Cambridge University Press:  14 April 2009

Trudy F. C. Mackay
Trudy F. C. Mackay
Affiliation:
Department of Genetics, University of Edinburgh, West Mains Road, Edinburgh EH9 3JN, U.K.
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P element mutagenesis was used to contaminate M strain second chromosomes with P elements. The contaminated lines were compared to uncontaminated control lines for homozygous and heterozygous fitness and its components. Mean homozygous fitness, viability and fertility of chromosome lines contaminated with P elements is decreased relative to the uncontaminated control lines by, respectively, 55, 28 and 40%. Variance among contaminated homozygous lines of total fitness increases by a factor of 1·5, variance of viability by a factor of 5·9, and variance of fertility by a factor of 1·9, compared to variance of these traits among the population of uncontaminated homozygous chromosomes. Estimates of P-element-induced mutational variance among second chromosome lines for homozygous fitness, viability and fertility are, respectively, 2 × 10−2, 5 × 10−2 and 2 × 10−2. This magnitude of mutational effect is equivalent, in terms of incidence of induced recessive lethal chromosomes and D:L ratio, to a dose of approximately 1·0–2·5 × 10−3 m EMS. The distributions of fitness traits among M-derived second chromosome homozygous lines contaminated with P elements are remarkably similar in many regards to distributions of fitness and viability of chromosomal homozygotes derived from natural Drosophila populations. It is possible that a proportion of the fitness variation previously observed (reviewed by Simmons & Crow, 1977) following homozygosis of wild chromosomes was not present in the natural populations, but was generated by P-element transposition during the chromosome extraction procedure. P-element-induced fitness mutations appear to be completely recessive. Implications for models of evolution of transposable elements are discussed.

Type
Research Article
Information
Genetics Research , Volume 48 , Issue 2 , October 1986 , pp. 77 - 87
Copyright
Copyright © Cambridge University Press 1986

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