Y-linked variation for autosomal immune gene regulation has the potential to shape sexually dimorphic immunity
Author(s) -
Ian C. Kutch,
Kenneth M. Fedorka
Publication year - 2015
Publication title -
proceedings of the royal society b biological sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.342
H-Index - 253
eISSN - 1471-2954
pISSN - 0962-8452
DOI - 10.1098/rspb.2015.1301
Subject(s) - biology , sexual dimorphism , genetics , gene , melanogaster , drosophila melanogaster , immune system , phenotype , x chromosome , regulation of gene expression , population , evolutionary biology , demography , sociology , endocrinology
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.
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