Relationships between the polygenes affecting the rate of development and viability in Drosophila melanogaster.

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  • YOSHIMARU Hiroshi
    Laboratory of Population Genetics, Department of Biology, Faculty of Science, Kyushu University Department of Epidemiology, Kyorin Unviersity School of Health Sciences
  • MUKAI Terumi
    Laboratory of Population Genetics, Department of Biology, Faculty of Science, Kyushu University

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  • キイロショウジョウバエにおける発育速度と生存力を支配するポリジーンの相互関係〔英文〕
  • キイロショウジョウバエ ニ オケル ハツイク ソクド ト セイゾンリョク オ

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Abstract

The polygenes affecting developmental rate were characterized and its role in natural populations was investigated. Using the second chromosome lines of Drosophila melanogaster in which genetic variation is entirely due to newly arisen mutations and those extracted from the Ishigakijima natural population, several experiments were conducted, and the following findings were obtained: (1) The minimum estimate of spontaneous mutation rate was 0.148 per second chromosome per generation. This estimate is similar to that of viability polygenes (0.14, Mukai 1964). (2) The maximum estimate of homozygous effect of a mutant polygene was 0.0095, which is slightly smaller than the average effect of viability polygenes (0.027, Mukai 1964). (3) The average degree of dominance of newly arisen mutant polygenes was 0.400. This is nearly equal to that of viability polygenes (0.41, Mukai and Yamazaki 1968). The average degree of dominance of the genes in question which experienced natural selection was estimated to be 0.150 in the Ishigakijima population. It is slightly smaller than that of viability polygenes (0.21, Tachida et al. 1983). (4) Positive genotypic correlations between developmental rates and viabilities were observed for not only the chromosomes having newly arisen mutations but also those extracted from a natural population. The above (1) and (4) may indicate that the change of developmental rate is a pleiotropic effect of viability polygenes. (5) The above findings suggest mutation-selection balance as the main mechanism of maintenance of genetic variation in developmental rate.

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