Y-Linked Variation For Autosomal Immune Gene Regulation Has The Potential To Shape Sexually Dimorphic Immunity

Keywords

Fitness; Gene expression; Serratia marcescens; Sexual dimorphism; Y-linked regulatory variation

Abstract

Sexually dimorphic phenotypes arise from the differential expression of male and female shared genes throughout the genome. Unfortunately, the underlying molecular mechanisms by which dimorphic regulation manifests and evolves are unclear. Recent work suggests that Y-chromosomes may play an important role, given that Drosophila melanogaster Ys were shown to influence the regulation of hundreds of X and autosomal genes. For Y-linked regulatory variation (YRV) to facilitate sexually dimorphic evolution, however, it must exist within populations (where selection operates) and influence male fitness. These criteria have seldom been investigated, leaving the potential for dimorphic evolution via YRV unclear. Interestingly, male and female D. melanogaster differ in immune gene regulation. Furthermore, immune gene regulation appears to be influenced by the Y-chromosome, suggesting it may contribute to dimorphic immune evolution.We address this possibility by introgressing Y-chromosomes from a single wild population into an isogenic background (to create Y-lines) and assessing immune gene regulation and bacterial defence. We found that Y-line males differed in their immune gene regulation and their ability to defend against Serratia marcescens. Moreover, gene expression and bacterial defence were positively genetically correlated. These data indicate that the Y-chromosome has the potential to shape the evolution of sexually dimorphic immunity in this system.

Publication Date

12-2-2015

Publication Title

Proceedings of the Royal Society B: Biological Sciences

Volume

282

Issue

1820

Document Type

Article

Personal Identifier

scopus

DOI Link

https://doi.org/10.1098/rspb.2015.1301

Socpus ID

84951745269 (Scopus)

Source API URL

https://api.elsevier.com/content/abstract/scopus_id/84951745269

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