The level and distribution of genetic variability within and among Metrosideros polymorpha populations along altitudinal gradients on the island of Maui, Hawaii were examined to assess the extent of genetic differentiation. Sixteen loci encoding 11 enzymes were scored in 17 populations along the NE wet slope of Mt. Haleakala and Kipahulu Valley in East Maui and six populations along the Puu Kukui trail in West Maui. On average, 50% of the loci were polymorphic within populations with an overall mean of 2·15 alleles per locus. The observed heterozygosities for different populations were moderate (0·108–0·220) and conformed to panmixia except for one of the mid-elevation populations. The distribution of allozyme variation indicates that very little differentiation has occurred along altitudinal gradients. Approximately 90% of the total variation resides within populations in East Maui while 95% was found within West Maui populations. The mean populational pair-wise genetic identities (Nei's I) ranged from 0·909 to 0·998. The UPGMA cluster analysis on genetic identity matrices and PCA on allele frequencies revealed marginal altitudinal differentiation. Twenty one alleles out of a total 63 showed statistically significant correlations with environmental variables.

We have described a new unstable mutant of the vestigial locus isolated from a natural population. From this mutant, vestigialalmost (vgal), wild-type (vgal+), and extreme (vgext), alleles arose spontaneously. The molecular analysis of vgal shows that the mutation is due to a 1874 bp hobo element inserted in a vestigial intron. Two distinct kinds of events lead a wild-type phenotype. Three independent vgal+ alleles result from an excision of the hobo element and two other vgal+ alleles have further deletions of hobo sequence. The sequence of one of them shows a 1516 bp hobo insertion at the same place and in the same orientation as the 1874 bp insertion. In the vgext alleles, we found a 5′ or 3′ variably sized deletion of vg sequences. One of them, which has been cloned and sequenced, has a deletion finishing exactly at the left terminal repeat′ hobo element. The genetic implications of these different genetic structures are discussed.

X chromosomes derived from crosses of inbred P and M Drosophila melanogaster strains that had extreme effects on abdominal and/or sternopleural bristle number in males, were further analyzed to determine their effects in females and to map the loci at which the mutations occurred. Seven lines that had on average 3.9 fewer sternopleural bristles than wildtype in males had average homozygous sternopleural bristle effects of −2·2. The bristle effects were partially recessive, with an average degree of dominance of −0·60. Physical mapping of the sternopleural bristle effects of these lines placed them all at approximately 24·7 cM. These mutations are apparently allelic on the basis of a complementation test, and deficiency mapping indicates they occur within chromosomal bands 8A4; 8C6. In situ hybridization analysis of the sites of P element insertions of these lines suggests that mutations probably resulted from excision of P elements at 8C on the original inbred P strain chromosome. Two additional lines, NDC(19) and DP(146), had reduced numbers of sternopleural and abdominal bristles. NDC(19) males had 9·7 fewer abdominal and 8·6 fewer sternopleural bristles than wildtype. The corresponding homozygous abdominal and sternopleural bristle number effects were −5·8 and −3·8, respectively; with the abdominal bristle effect completely recessive and the sternopleural bristle effect nearly additive. DP(146) males had 6·2 fewer abdominal and 4·1 fewer sternopleural bristles than wildtype, with homozygous abdominal bristle effects of −4·3 and sternopleural bristle effects of −2·0. Abdominal bristle effects of this line were partially recessive whereas the sternopleural bristle effects were additive. Physical mapping showed effects on both bristle traits segregated jointly in these two lines, with the NDC(19) mutation closely linked to y and the DP(146) mutation 0·17 cM from it. Complementation tests and deficiency mapping also indicate the mutations in lines NDC(19) and DP(146) are at closely linked but separate loci within chromosomal bands 1B2; 1B4–6 and 1B4–6; 1B10 respectively, with some epistatic effects. In situ hybridization analysis of sites of P element insertion suggest that the NDC(19) mutation, which may be a scute allele, was probably caused by a P element insertion in the IB region; the DP(146) mutation is also associated with an insertion at IB.

We have determined 1990 bp mitochondrial DNA sequence which extends from 3′ end of the cytochrome oxidase subunit I (COI) gene to 5′ end of the COIII gene from two sibling species of Drosophila, D. simulans and D. mauritiana. Analyses of the sequences and part of the NADH dehydrogenase subunit 2 gene and the COI gene together with those from D. melanogaster and D. yakuba revealed that amino-acid substitution rate of the ATPase 6 gene seems to be higher in some strains of D. melanogaster than in the other species. High level of amino-acid polymorphism in this gene was observed in D. melanogaster. Synonymous substitution rate is relatively constant in all the genes examined, suggesting that mutation rate is not higher in the ATPase 6 gene of D. melanogaster. The amino-acid substitutions found specifically in D. melanogaster are at the sites which are not conserved among mammals, yeast and E. coli. These sites of the ATPase 6 gene might lose the selective constraint in D. melanogaster, and the amino-acid substitutions can be explained by neutral mutations and random genetic drift.

Models of the evolutionary advantages of sex and genetic recombination due to directional selection on a quantitative trait are analysed. The models assume that the trait is controlled by many additive genes. A nor-optimal selection function is used, in which the optimum either moves steadily in one direction, follows an autocorrelated linear Markov process or a random walk, or varies cyclically. The consequences for population mean fitness of a reduction in genetic variance, due to a shift from sexual to asexual reproduction are examined. It is shown that a large reduction in mean fitness can result from such a shift in the case of a steadily moving optimum, under light conditions. The conditions are much more stringent with a cyclical or randomly varying environment, especially if the autocorrelation for a random environment is small. The conditions for spread of a rare modifier affecting the rate of genetic recombination are also examined, and the strength of selection on such a modifier determined. Again, the case of a steadily moving optimum is most favourable for the evolution of increased recombination. The selection pressure on a recombination modifier when a trait is subject to strong truncation selection is calculated, and shown to be large enough to account for observed increases in recombination associated with artificial selection. Theoretical and empirical evidence relevant to evaluating the importance of this model for the evolution of sex and recombination is discussed.

Asexual populations experiencing random genetic drift can accumulate an increasing number of deleterious mutations, a process called Muller's ratchet. We present here diffusion approximations for the rate at which Muller's ratchet advances in asexual haploid populations. The most important parameter of this process is n0 = N e−U/s, where N is population size, U the genomic mutation rate and s the selection coefficient. In a very large population, n0 is the equilibrium size of the mutation-free class. We examined the case n0 > 1 and developed one approximation for intermediate values of N and s and one for large values of N and s. For intermediate values, the expected time at which the ratchet advances increases linearly with n0. For large values, the time increases in a more or less exponential fashion with n0. In addition to n0, s is also an important determinant of the speed of the ratchet. If N and s are intermediate and n0 is fixed, we find that increasing s accelerates the ratchet. In contrast, for a given n0, but large N and s, increasing s slows the ratchet. Except when s is small, results based on our approximations fit well those from computer simulations.