No effect of mitochondrial genotype on reproductive plasticity following exposure to a non-infectious pathogen challenge in female or male Drosophila

Abstract

Mitochondrial genetic variation shapes the expression of life-history traits associated with reproduction, development and survival, and has also been associated with the prevalence and progression of infectious bacteria and viruses in humans. The breadth of these effects on multifaceted components of health, and their link to disease susceptibility, led us to test whether variation across mitochondrial haplotypes affected reproductive success following an immune challenge in the form of a non-infectious pathogen. We test this, by challenging male and female fruit flies (Drosophila melanogaster), harbouring each of three distinct mitochondrial haplotypes in an otherwise standardized genetic background, to either a mix of heat-killed bacteria, or a procedural control, prior to measuring their subsequent reproductive performance. The effect of the pathogen challenge on reproductive success did not differ across mitochondrial haplotypes; thus there was no evidence that patterns of reproductive plasticity were modified by the mitochondrial genotype following a non-infectious pathogen exposure. We discuss the implications of our data, and suggest future research avenues based on these results.

Figure 1. Effect of pathogen treatment and mitochondrial strain on reproductive success (cumulative mean ± SE).

Numbers above SE denote effect sizes of treatment vs. control per haplotype. (a) Female reproductive success, n = [pathogen challenge/control]: Japan = [23/19], Israel = [22/23], Dahomey = [21/21]. (b) Male reproductive success, n = [pathogen challenge/control]: Japan = [24/22], Israel = [22/26,] Dahomey = [17/19].

Figure 2. Effect of pathogen treatment on reproductive success across four days of ovipositing (X ± SE).

Note that the focal females (a) and males (b) are increasing in age across the four day mating assay, whereas the tester females and males are kept at a standardized (3–4 d) age throughout. (a) Female reproductive success, N_individuals = [pathogen challenge/control]: [66/63]. (b) Male reproductive success, N_individuals = [pathogen challenge/control]: [63/67].

Figure 3. Effect of female age of mating (three days vs. four days) on total number of eclosed offspring (means [diamond symbol] ± SE displayed inside box plots).

Figure 4. Outline of experimental design for both sexes.

Females were transferred to new ovipositing vials every 24 h, each of which was retained for eleven days, at which point eclosing offspring were counted.