Abstract
Three populations of Drosophila melanogaster that were daughter populations of two others with histories of high, continuous radiation exposure [population 5 (irradiated, small population size) gave rise to populations 17 (small) and 18 (large); population 6 (irradiated, large population size) gave rise to population 19 (large)] were maintained for 1 year with no radiation exposure. The frequency with which random combinations of second chromosomes taken from population 19 proved to be lethal changed abruptly after about 8 months, thus revealing the origin of a selectively favored element in that population. (This "element" may or may not have been the cause of the lethality.) A comparison of the loss of lethals in populations 17 and 18 with a loss that occurred concurrently in the still-irradiated population 5 suggests that a second, selectively favored element had arisen in that population just before populations 17 and 18 were split off. This element was on a nonlethal chromosome. The result in population 5 was the elimination of many lethals from that population, followed by a subsequent increase as mutations occurred in the favored nonlethal chromosome. Populations 17 and 18, with no radiation exposure, underwent a loss of lethals with no subsequent increase. The events described here, as well as others to be described elsewhere, suggest that populations may be subject to episodic periods of rapid gene frequency changes that occur under intense selection pressure. In the instances in which the changeover was revealed by the elimination of preexisting lethals, earlier lethal frequencies were reduced by approximately one-half; the selectively favored elements appear, then, to be favored in the heterozygous--not homozygous--condition.
Full text
PDF
Selected References
These references are in PubMed. This may not be the complete list of references from this article.
- ATWOOD K. C., SCHNEIDER L. K., RYAN F. J. Selective mechanisms in bacteria. Cold Spring Harb Symp Quant Biol. 1951;16:345–355. doi: 10.1101/sqb.1951.016.01.026. [DOI] [PubMed] [Google Scholar]
- Allen D. J., Rickinson A. B., Wallace L. E., Rowe M., Moss D. J., Epstein M. A. Stimulation of human lymphocytes with irradiated cells of the autologous Epstein-Barr virus-transformed cell line. II. Cytotoxic response to repeated stimulation. Cell Immunol. 1982 Feb;67(1):141–151. doi: 10.1016/0008-8749(82)90206-4. [DOI] [PubMed] [Google Scholar]
- Crow J. F. Alternative Hypotheses of Hybrid Vigor. Genetics. 1948 Sep;33(5):477–487. doi: 10.1093/genetics/33.5.477. [DOI] [PMC free article] [PubMed] [Google Scholar]
- MULLER H. J. Our load of mutations. Am J Hum Genet. 1950 Jun;2(2):111–176. [PMC free article] [PubMed] [Google Scholar]
- NOVICK A., SZILARD L. Experiments with the Chemostat on spontaneous mutations of bacteria. Proc Natl Acad Sci U S A. 1950 Dec;36(12):708–719. doi: 10.1073/pnas.36.12.708. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Wallace B., Kass T. L. On the structure of gene control regions. Genetics. 1974 Jul;77(3):541–558. doi: 10.1093/genetics/77.3.541. [DOI] [PMC free article] [PubMed] [Google Scholar]