Gao Ke, van der Heide Wout, Muijderman Daphne, Nichols Sarah, Karwal Carmen, Kuperus Peter, Groot Astrid T
Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, Amsterdam, the Netherlands.
Department of Cell and Developmental Biology, University of California San Diego, La Jolla, California, USA.
Insect Sci. 2025 Feb;32(1):290-300. doi: 10.1111/1744-7917.13379. Epub 2024 May 20.
Given 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.
正如免疫能力缺陷假说（ICHH）所假定的那样，鉴于自然界中资源的可用性有限，性吸引力可能会与免疫能力相互权衡。在无脊椎动物中，到目前为止尚未发现通过性信号中的激素/分子效应器进行权衡与免疫之间的直接联系。在这里，我们评估了性信号的变化如何影响绿铃夜蛾（Chloridea virescens）两个经性信息素选择的品系中的寄生虫感染：一个具有低16:Ald/Z11-16:Ald比例的有吸引力品系和一个具有高比例的无吸引力品系。当用一种顶复门寄生虫感染这些品系时，我们发现有吸引力的低比例品系比无吸引力的高比例品系对寄生虫感染的易感性显著更高。由于这两个品系之间的比例差异由一种δ-11-去饱和酶决定，我们推测这种去饱和酶可能具有双重作用，即在性信号质量方面以及参与免疫反应，这与脊椎动物中的睾酮类似。然而，当我们使用CRISPR/cas9敲除有吸引力的低比例品系中的δ-11-去饱和酶时，我们发现其信息素表型确实转变为高比例品系的表型，但感染易感性并未改变。值得注意的是，当检查绿铃夜蛾中δ-11-去饱和酶的基因组位置时，我们发现粘蛋白与δ-11-去饱和酶相邻。当比较两个品系中的粘蛋白序列时，我们在编码序列中发现了四个非同义单核苷酸多态性，以及两个品系之间的内含子变异。这些差异表明遗传搭便车可能解释了对寄生虫感染易感性的变化。
