Genetics, Vol. 163, 1357-1364, April 2003, Copyright © 2003

Dominance of Mutations Affecting Viability in Drosophila melanogaster

James D. Frya and Sergey V. Nuzhdinb
a Department of Biology, University of Rochester, Rochester, New York 14627
b Section of Evolution and Ecology, University of California, Davis, California 95616

Corresponding author: James D. Fry, University of Rochester, Rochester, NY 14627-0211., jfry{at}mail.rochester.edu (E-mail)

Communicating editor: W. STEPHAN

There have been several attempts to estimate the average dominance (ratio of heterozygous to homozygous effects) of spontaneous deleterious mutations in Drosophila melanogaster, but these have given inconsistent results. We investigated whether transposable element (TE) insertions have higher average dominance for egg-to-adult viability than do point mutations, a possibility suggested by the types of fitness-depressing effects that TEs are believed to have. If so, then variation in dominance estimates among strains and crosses would be expected as a consequence of variation in TE activity. As a first test, we estimated the average dominance of all mutations and of copia insertions in a set of lines that had accumulated spontaneous mutations for 33 generations. A traditional regression method gave a dominance estimate for all mutations of 0.17, whereas average dominance of copia insertions was 0.51; the difference between these two estimates approached significance (P = 0.08). As a second test, we reanalyzed OHNISHI 1974 Down data on dominance of spontaneous and EMS-induced mutations. Because a considerable fraction of spontaneous mutations are caused by TE insertions, whereas EMS induces mainly point mutations, we predicted that average dominance would decline with increasing EMS concentration. This pattern was observed, but again fell short of formal significance (P = 0.07). Taken together, however, the two results give modest support for the hypothesis that TE insertions have greater average dominance in their viability effects than do point mutations, possibly as a result of deleterious effects of expression of TE-encoded genes.





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