Abstract
An extremely large detrimental to lethal load ratio (D/L ratio) of homozygous viability was detected in the Osaka natural population of Drosophila melanogaster in 1979. Mutations were accumulated on 79 second chromosome lines that originated from one of the Osaka isogenic second chromosome lines. After five generations the genetic load and ADH specific activity were measured. The results suggest that a putative transposon which is tentatively called "MY factor" induced an extremely high frequency of mutations most probably in non-coding regions, and that some of these mutations modify the ADH specific activity.
