PgmNr D1180: Functional consequences of a selfish X-chromosome in Drosophila neotestacea.

Authors:
K. Pieper 1 ; K. Dyer 1 ; R. Unckless 2


Institutes
1) The University of Georgia, Athens, GA; 2) University of Kansas, Lawrence, KS.


Keyword: spermatogenesis

Abstract:

Genetic conflict is ubiquitous across the tree of life and can have significant consequences for the genome. The sex-ratio X-chromosome (SR) of the fruit fly Drosophila neotestacea is a selfish sex chromosome that promotes its own transmission at the expense of the Y-chromosome. In the testes of males that carry SR, half of the sperm fail to develop through an unknown mechanism and thus no Y-bearing sperm are produced. The offspring of these males are nearly all daughters, with the only sons being sterile X0 males. SR produces this selfish phenotype equally strongly against all tested genetic backgrounds, and there are no known phenotypic effects other than halved sperm production in males. Our goals are to characterize the mechanism of the SR phenotype, identify candidates for the causal loci on the SR chromosome, and understand the downstream effects of SR. As a first step, we performed whole transcriptome sequencing of the testes and carcass (whole body minus testes) of SR-carrying males and males carrying the standard X-chromosome. We compared gene expression levels to find transcripts differentially expressed in the testes of SR males but not the carcass, which are candidates for involvement in the selfish mechanism. Transcripts that are on the X-chromosome are particularly strong candidates for the causal loci, whereas autosomal genes that are differentially expressed in the testes may be activated downstream of the SR mechanism or regulated in trans by genes located on SR. Genes that are differentially expressed in the carcass may represent previously unknown pleiotropic consequences of SR. We also examine the differential expression of genes already known to be involved in different stages of spermatogenesis to identify when the SR mechanism activates to cause developmental failure. Overall, our results quantify the functional consequences of SR, identify potential candidates for the molecular mechanism, and lay a foundation for future investigations of the evolutionary genomic consequences of genetic conflict.