The maintenance of reproductive fitness in lines subjected to artificial selection is one of the major problems in animal breeding. The decline in reproductive performance has neither been predictable from heritabilities and genetic correlations, nor have conventional selection indices been adequate to avoid the problem. Gowe (1983) has suggested that the heritabilities of reproductive traits are non-linear, with heritabilities being higher on the lower fitness side. Consequently, he has predicted that culling on reproductive fitness in artificial selection lines will be effective in preventing the usual declines in fitness. An experimental evaluation of Gowe's prediction has been carried out by comparing fitnesses of replicated lines of three treatments: selection for increased inebriation time without culling on fitness (HO), selection for inebriation time with culling of 20% (4/20) of selected females on reproductive fitness (HS), and unselected controls (C). Response to selection for inebriation time in the two selection treatments was similar. After 25 generations, the competitive index, a measure of reproductive fitness, was significantly lower in the HO treatment than the HS treatment, while the HS treatment did not differ from the control lines or the base population. These results demonstrate for the first time that culling on reproductive fitness in selection lines can be used to prevent the usual decline in reproductive performance.
The response to long-term selection for increased abdominal bristle number was studied in six replicate lines of Drosophila melanogaster derived from the sc Canberra outbred strain. Each line was continued for 86-89 generations with 50 pairs of parents selected at an intensity of 20 %, and subsequently for 32-35 generations without selection. Response continued for at least 75 generations and average total response was in excess of 36 additive genetic standard deviations of the base population (cr A ) or 51 times the response in the first generation. The pattern of longterm response was diverse and unpredictable typically with one or more accelerated responses in later generations. At termination of the selection, most of the replicate lines were extremely unstable with high phenotypic variability, and lost much of their genetic gains rapidly upon relaxation of selection.The variation in response among replicates rose in the early phase of selection to level off at approximately 7-6 a\ around generation 25. As some lines plateaued, it increased further to a level higher than would be accommodated by most genetic models. The replicate variation was even higher after many generations of relaxed selection. The genetic diversity among replicates, as revealed in total response, the individuality of response patterns and variation of the sex-dimorphism ratio, suggests that abdominal bristle number is influenced potentially by a large number of genes, but a smaller subset of them was responsible for selection response in any one line.
Lethal frequencies on the second and third chromosomes were estimated three times in six replicate lines of Drosophila melanogaster selected for increased abdominal bristle number, at G 14-16, G 37-44 and G 79. Ten lethals were detected at a frequency of about 5 % or higher at G 14-16, of which only one recurred in subsequent tests. Another ten lethals which had not been detected previously were found at G 37-44, and the 5 most frequent ones recurred at G 79. In the last test, 15 presumably new lethals were detected, of which at least 4 appeared well established. In addition, six reversions (from sc to sc+), a new mutant at the scute locus and sea were discovered. The effects on the selected character of some lethals and visible mutants were large and variable, but not always sufficient to explain the observed frequencies. The major lethals detected at G 37-44 and G 79 for the first time were most probably 'mutations' (in the broad sense) which occurred during selection. The likely origins of such ' mutations' were discussed, with a suggestion that the known mutation rate for recessive lethals would not be incompatible with the observed frequency of occurrence of the 'mutations'.
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