Summary 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.
No takes yet. Share an insight, caveat, or question.
Trudy F. C. Mackay (1986) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: