Genetics and genomics of
            <i>Drosophila</i>
            mating behavior

Mackay, Trudy F. C.; Heinsohn, Stefanie L.; Lyman, Richard F.; Moehring, Amanda J.; Morgan, Theodore J.; Rollmann, Stephanie M.

doi:10.1073/pnas.0501986102

Cited by 133 publications

(146 citation statements)

References 87 publications

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“…This suggests that a heritable change in female behaviour has taken place, rather than a change in the interaction between males and females. Our results are comparable to those in a selection experiment with D. melanogaster (Mackay et al 2005).…”

Section: Discussionsupporting

confidence: 80%

“…Females from high receptivity lines hybridized more frequently with Drosophila simulans males, a result that mirrored the earlier finding that artificial selection for hybridization between these two species resulted in D. melanogaster females showing increased receptivity (Carracedo et al 1991). Another study on D. melanogaster found an asymmetric response to selection on mating speed, in 29 generations, with females from the slow lines reducing their receptivity (Mackay et al 2005). Estimates of realized heritability averaged 7%.…”

Section: Discussionsupporting

confidence: 67%

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Laboratory evolution of polyandry in the parasitoid wasp Nasonia vitripennis

et al. 2007

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Section: Discussionsupporting

confidence: 80%

Section: Discussionsupporting

confidence: 67%

Laboratory evolution of polyandry in the parasitoid wasp Nasonia vitripennis

et al. 2007

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“…To further test the hypothesis that hemizygosity mediates faster evolution in response to selection, we compared genes with additive variation attributable to the X in males to a list of genes whose expression differed between lines selected for mating speed and controls in D. melanogaster (22). We found that selection response was more frequently attributable to genes with our predicted fast evolving genes than expected by chance (P ϭ 8.3 ϫ 10 Ϫ11 ; SI Data Set 3).…”

Section: Discussionmentioning

confidence: 99%

Simpler mode of inheritance of transcriptional variation in maleDrosophila melanogaster

Wayne

Telonis‐Scott

Bono

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Sexual selection drives faster evolution in males. The X chromosome is potentially an important target for sexual selection, because hemizygosity in males permits accumulation of alleles, causing tradeoffs in fitness between sexes. Hemizygosity of the X could cause fundamentally different modes of inheritance between the sexes, with more additive variation in males and more nonadditive variation in females. Indeed, we find that genetic variation for the transcriptome is primarily additive in males but nonadditive in females. As expected, these differences are more pronounced on the X chromosome than the autosomes, but autosomal loci are also affected, possibly because of X-linked transcription factors. These differences may be of evolutionary significance because additive variation responds quickly to selection, whereas nonadditive genetic variation does not. Thus, hemizygosity of the X may underlie much of the faster male evolution of the transcriptome and potentially other phenotypes. Consistent with this prediction, genes that are additive in males and nonadditive in females are overrepresented among genes responding to selection for increased mating speed.microarray ͉ sexual antagonism ͉ sexual conflict ͉ sexual selection ͉ transcription

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“…A mutation in muscleblind is associated with increased aggression (Edwards et al 2006) and increased resistance to the inebriating effects of ethanol (Morozova et al 2007), but reduced locomotor startle response (Jordan et al 2007). Independent evidence for pervasive pleiotropy comes from the substantial overlap of transcripts for which there are correlated responses in expression to selection from the same base population for copulation latency, aggressive behavior, locomotor startle response, and ethanol resistance (Mackay et al 2005;Edwards et al 2006;Jordan et al 2007;Morozova et al 2007).…”

Section: Genetic Architecture: Pleiotropymentioning

confidence: 99%

Genetic architecture of quantitative traits in mice, flies, and humans

Flint¹,

Mackay²

2009

Genome Res.

409

364

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We compare and contrast the genetic architecture of quantitative phenotypes in two genetically well-characterized model organisms, the laboratory mouse, Mus musculus, and the fruit fly, Drosophila melanogaster, with that found in our own species from recent successes in genome-wide association studies. We show that the current model of large numbers of loci, each of small effect, is true for all species examined, and that discrepancies can be largely explained by differences in the experimental designs used. We argue that the distribution of effect size of common variants is the same for all phenotypes regardless of species, and we discuss the importance of epistasis, pleiotropy, and gene by environment interactions. Despite substantial advances in mapping quantitative trait loci, the identification of the quantitative trait genes and ultimately the sequence variants has proved more difficult, so that our information on the molecular basis of quantitative variation remains limited. Nevertheless, available data indicate that many variants lie outside genes, presumably in regulatory regions of the genome, where they act by altering gene expression. As yet there are very few instances where homologous quantitative trait loci, or quantitative trait genes, have been identified in multiple species, but the availability of high-resolution mapping data will soon make it possible to test the degree of overlap between species.Recent successes in mapping quantitative trait loci (QTLs) that contribute to phenotypic variation in humans and model organisms make it possible to address important questions about the genetic architecture of quantitative phenotypes, such as the likely number of loci, their mode of genetic action, and interaction with each other and with the environment. An understanding of the genetic architecture of quantitative traits is not only important in its own right, it will also inform studies that seek to proceed to the identification of the quantitative trait genes (QTGs) and the quantitative trait nucleotide (QTN) variants, the functional changes in DNA sequence that contribute to trait variation.In this work we use examples from two genetically wellcharacterized model organisms, the laboratory mouse, Mus musculus, and the fruit fly, Drosophila melanogaster, to discuss how an understanding of the genetic architecture of quantitative phenotypes in model organisms informs mapping experiments in human genetics. In our discussion of the latter, we draw upon the recent successful application of genome-wide association studies (GWAS) to both quantitative phenotypes (such as height and weight) and disease phenotypes (assuming that the genetic architecture of common disease is similar, if not identical, to that of quantitative phenotypes).Genetic architecture has been the subject of a number of recent reviews, most of which deal with information from a single model organism (Mackay 2004) or review a small number of phenotypes (Kendler and Greenspan 2006). Here, our purpose is different. We tackle three relate...

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Genetics and genomics of Drosophila mating behavior

Cited by 133 publications

References 87 publications

Laboratory evolution of polyandry in the parasitoid wasp Nasonia vitripennis

Laboratory evolution of polyandry in the parasitoid wasp Nasonia vitripennis

Simpler mode of inheritance of transcriptional variation in maleDrosophila melanogaster

Genetic architecture of quantitative traits in mice, flies, and humans

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