No abstract

Spontaneous mutations were allowed to accumulate in a second chromosome that was transmitted only through heterozygous males for 40 generations. At 10-generation intervals the chromosomes were assayed for homozygous effects of the accumulated mutants. From the regression of homozygous viability on the number of generations of mutant accumulation and from the increase in genetic variance between replicate chromosomes it is possible to estimate the mutation rate and average effect of the individual mutants. Lethal mutations arose at a rate of 0.0060 per chromosome per generation. The mutants having small effects on viability are estimated to arise with a frequency at least 10 times as high as lethals, more likely 20 times as high, and possibly many more times as high if there is a large class of very nearly neutral mutations.—The dominance of such mutants was measured for chromosomes extracted from a natural population. This was determined from the regression of heterozygous viability on that of the sum of the two constituent homozygotes. The average dominance for minor viability genes in an equilibrium population was estimated to be 0.21. This is lower than the value for new mutants, as expected since those with the greatest heterozygous effect are most quickly eliminated from the population. That these mutants have a disproportionately large heterozygous effect on total fitness (as well as on the viability component thereof) is shown by the low ratio of the genetic load in equilibrium homozygotes to that of new mutant homozygotes.

Within-line heterogeneity has been found in the mitochondrial DNA (mtDNA) in two isofemale lines of D. simulans. The co-existing types, S and M, were typical of the mtDNA in D. simulans and in D. mauritiana, respectively, their nucleotide divergence per site being ca. 2-1 %. Segregation analysis confirmed that some individuals in these lines were heteroplasmic and suggested incomplete maternal inheritance of mtDNA in Drosophila. Examination of other lines of D. simulans revealed that the M type of D. mauritiana occurs at 71 % in Reunion, 38% in Madagascar and 0 % in Kenya. This finding and interspecific sequence comparisons of both M types indicate that D. mauritiana diverged from D. simulans probably less than 240000 years ago.

461 second chromosomes of Drosophila melanogaster were extracted from a Raleigh, N.C. population and four enzymes controlled by the genes located in this chromosome (alcohol dehydrogenase (EC 1.1.1.1.), malate dehydrogenase-1 (EC 1.1.1.37), glycerol-3-phosphate dehydrogenase-1 (EC 1.1.1.8), and α-amylase (EC 3.2.1.1), were assayed electrophoretically and cytologically (salivary-gland chromosomes). Linkage disequilibrium could not be detected among any pair of isozyme genes, except in one case that is best explained as due to a chance error in estimation. Some disequilibria were detected, however, between isozyme genes and polymorphic inversions. The relative viabilities of homozygous and heterozygous combinations of these chromosomes were estimated with respect to the alcohol dehydrogenase alleles and the glycerol-3-phosphate dehydrogenase alleles; no significant difference could be detected. The role of epistasis in natural populations is discussed on the basis of these results.