caa a22 4500 386393230 CHVBK 20180307112127.0 cr unu---uuuuu 161130e198904 xx s 000 0 eng 10.1017/S0016672300028019 doi S0016672300028019 pii (NATIONALLICENCE)cambridge-10.1017/S0016672300028019 Can chromosomal heterosis in Drosophila be explained by deleterious recessive genes? Negative results from a dichromosomal population test [Elektronische Daten] High levels of chromosomal heterosis have previously been detected in Drosophila using the balancer chromosome equilibration (BE) technique, in which single wild-type chromosomes are introduced into population cages along with a dominant/lethal balancer chromosome. The balancer chromosome is rarely eliminated in such populations, showing that the fitness of chromosome homozygotes must be low by comparison with chromosomal heterozygotes. As with all cases of chromosomal heterosis, the underlying cause could either be deleterious recessives at various loci or generalized overdominance. The experiment of the present paper examines the first of these explanations. Population cages containing just two wild-type chromosomes (dichromosomal populations) were set up and allowed to run for many generations. Single chromosomes were then re-extracted from these populations, and their fitness measured using the BE technique. Our expectation was that the gradual elimination of recessive genes from the dichromosomal populations ought to result in an increase in the fitness of such re-extracted chromosome homozygotes. Yet in two replicated experiments we were unable to demonstrate an; unequivocal increase in fitness. We have estimated the rate of increase of fitness under multiple locus dominance and partial dominance models. The principal unknown parameter in these calculations is the selection intensity per locus, s. The expected increase is approximately proportional to s, and we estimate that values of s around 1/64 should be detectable in our experiments. However linkage is expected to reduce the efficiency of the dichromosomal procedure We show by computer simulation that this reduction is by a factor of approximately 2, thus increasing the detectable level of s to approximately 1/32. Consideration of mutation-selection balance models shows that this is a feasible selection intensity only if dominance is nearly complete. Thus we are unable to rule out the notion that the genes responsible for heterosis are maintained by a simple mutation-selection balance, but the experimental results constrain the parameters of such a model to a narrow range. Copyright © Cambridge University Press 1989 Wilton Alan N. School of Biological Sciences A12, University of Sydney, NSW 2006, Australia Joseph Michael G. School of Biological Sciences A12, University of Sydney, NSW 2006, Australia Sved John A. School of Biological Sciences A12, University of Sydney, NSW 2006, Australia Genetical Research Cambridge University Press 53/2(1989-04), 129-140 0016-6723 53:2<129 1989 53 GRH https://doi.org/10.1017/S0016672300028019 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1017/S0016672300028019 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Wilton Alan N. School of Biological Sciences A12, University of Sydney, NSW 2006, Australia NATIONALLICENCE 700 1- Joseph Michael G. School of Biological Sciences A12, University of Sydney, NSW 2006, Australia NATIONALLICENCE 700 1- Sved John A. School of Biological Sciences A12, University of Sydney, NSW 2006, Australia NATIONALLICENCE 773 0- Genetical Research Cambridge University Press 53/2(1989-04), 129-140 0016-6723 53:2<129 1989 53 GRH CC0 http://creativecommons.org/publicdomain/zero/1.0 nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-cambridge