Inversions fail to account for allozyme clines.

Allozyme and inversion data from natural populations of Drosophila melanogaster from the eastern United States were analyzed to determine whether the clines at allozyme loci are due to nonrandom associations with common cosmopolitan inversions. All inversions show strong clines. Clines were large and significant for half of the eight allozyme loci. An analysis of the contribution of inversions to clines of allozyme genes revealed three outcomes: the inversion cline (1) enhanced the allozyme cline, but was only partly responsible, (2) reduced the allozyme cline, and (3) had no effect. The allozyme clines were mainly determined by the pattern of allele frequencies within the chromosomal arrangements. Consequently, it was concluded that allozyme clines would exist in the absence of inversion clines.

Inversion Clines in Populations of DROSOPHILA MELANOGASTER.

Twenty different natural populations of Drosophila melanogaster were sampled to determine the frequencies of inversions. Based on their frequencies and geographical distributions, the inversions could be classified as follows: (1) Common cosmopolitan inversions that are present in many populations in frequencies exceeding five percent and that may exhibit frequency clines over large geographical regions; (2) Rare cosmopolitan inversions that occur throughout the species range but usually at frequencies below five percent and that may be absent in many populations; (3) Recurrent endemic inversions that are found in several adjacent populations in frequencies usually not exceeding one or two percent; and (4) Unique endemic inversions that are found only among the progeny of a single individual and that may represent one aspect of the syndrome termed "hybrid dysgenesis". Four common cosmopolitan inversions that exhibit highly significant clines in populations in the eastern United States are In(2L)t, In(2R)NS, In(3L)P and In(3R)P.

Mutation rate and dominance of genes affecting viability in Drosophila melanogaster.

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.

Linkage disequilibrium in a local population of Drosophila melanogaster.

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 alpha-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.