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Threshold trait architecture of Hsp90-buffered variation

Charles C. Carey, Kristen Gorman, Becky Howsmon, Aaron K. Aragaki, Charles Kooperberg, Suzannah Rutherford
doi: https://doi.org/10.1101/016980
Charles C. Carey
1Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA
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Kristen Gorman
1Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA
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Becky Howsmon
1Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA
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Aaron K. Aragaki
2Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA
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Charles Kooperberg
2Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA
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Suzannah Rutherford
1Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA
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  • For correspondence: srutherf@fhcrc.org
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Abstract

Common genetic variants buffered by Hsp90 are candidates for human diseases of signaling such as cancer. Like cancer, morphological abnormalities buffered by Hsp90 are discrete threshold traits with a continuous underlying basis of liability determining their probability of occurrence. QTL and deletion maps for one of the most frequent Hsp90-dependent abnormalities in Drosophila, deformed eye (dfe), were replicated across three genetically related artificial selection lines using strategies dependent on proximity to the dfe threshold and the direction of genetic and environmental effects. Up to 17 dfe loci (QTL) linked by 7 interactions were detected based on the ability of small recombinant regions of an unaffected and completely homozygous control genotype to dominantly suppress or enhance dfe penetrance at its threshold in groups of isogenic recombinant flies, and over 20 deletions increased dfe penetrance from a low expected value in one or more line, identifying a complex network of genes responsible for the dfe phenotype. Replicated comparisons of these whole-genome mapping approaches identified several QTL regions narrowly defined by deletions and 4 candidate genes, with additional uncorrelated QTL and deletions highlighting differences between the approaches and the need for caution in attributing the effect of deletions directly to QTL genes.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted March 25, 2015.
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Threshold trait architecture of Hsp90-buffered variation
Charles C. Carey, Kristen Gorman, Becky Howsmon, Aaron K. Aragaki, Charles Kooperberg, Suzannah Rutherford
bioRxiv 016980; doi: https://doi.org/10.1101/016980
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Threshold trait architecture of Hsp90-buffered variation
Charles C. Carey, Kristen Gorman, Becky Howsmon, Aaron K. Aragaki, Charles Kooperberg, Suzannah Rutherford
bioRxiv 016980; doi: https://doi.org/10.1101/016980

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