Ecological immunology: do sexual attraction and immunity trade‐off through a desaturase?

Author:

Gao Ke12ORCID,van der Heide Wout13ORCID,Muijderman Daphne1,Nichols Sarah1,Karwal Carmen4,Kuperus Peter1,Groot Astrid T.1

Affiliation:

1. Institute for Biodiversity and Ecosystem Dynamics University of Amsterdam Amsterdam the Netherlands

2. Department of Cell and Developmental Biology University of California San Diego La Jolla California USA

3. Department of Neurobiology and Behavior Cornell University Ithaca New York USA

4. University of Leiden Leiden the Netherlands

Abstract

AbstractGiven the limited availability of resources in nature, sexual attractiveness may trade off with immunocompetence, as the immunocompetence handicap hypothesis (ICHH) posits. In invertebrates, a direct link between trade‐offs through hormonal/molecular effectors in sexual signals and immunity has not been found so far. Here, we assessed how variation in sexual signals affected parasite infection in two sex pheromone selected lines of the moth Chloridea virescens: an attractive line with a low ratio of 16:Ald/Z11‐16:Ald and an unattractive line with a high ratio. When infecting these lines with an apicomplexan parasite, we found that the attractive Low line was significantly more susceptible to the parasite infection than the unattractive High line. Since the ratio difference between these two lines is determined by a delta‐11‐desturase, we hypothesized that this desaturase may have a dual role, i.e., in the quality of the sexual signal as well as an involvement in immune response, comparable to testosterone in vertebrates. However, when we used CRISPR/cas9 to knockout delta‐11‐desturase in the attractive Low line, we found that the pheromonal phenotype did change to that of the High line, but the infection susceptibility did not. Notably, when checking the genomic location of delta‐11‐desaturase in the C. virescens, we found that mucin is adjacent to delta‐11‐desaturase. When comparing the mucin sequences in both lines, we found four nonsynonymous SNPs in the coding sequence, as well as intronic variation between the two lines. These differences suggest that genetic hitchhiking may explain the variation in susceptibility to parasitic infection.

Funder

China Scholarship Council

National Science Foundation

Publisher

Wiley

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