Abstract
Spiroplasma poulsonii is a maternally transmitted bacterial endosymbiont that is naturally associated with Drosophila melanogaster. S. poulsonii resides extracellularly in the hemolymph, where it must acquire metabolites to sustain proliferation. In this study, we find that Spiroplasma proliferation specifically depletes host hemolymph diacylglyceride, the major lipid class transported by the lipoprotein, Lpp. RNAi-mediated knockdown of Lpp expression, which reduces the amount of circulating lipids, inhibits Spiroplasma proliferation demonstrating that bacterial proliferation requires hemolymph-lipids. Altogether, our study shows that an insect endosymbiont acquires specific lipidic metabolites from the transport lipoproteins in the hemolymph of its host. In addition, we show that the proliferation of this endosymbiont is limited by the availability of hemolymph lipids. This feature could limit endosymbiont over-proliferation under conditions of host nutrient limitation as lipid availability is strongly influenced by the nutritional state.
Highlights
Many insects harbor facultative bacterial endosymbionts, which despite not being required for host survival have important implications for host biology (Wernegreen, 2012)
These experiments demonstrate that (i) Spiroplasma has a low impact on the general fitness of its host, negatively affecting survival and egg laying only in old flies and (ii) that this decrease in host fitness correlates with higher Spiroplasma titers
We have demonstrated that Spiroplasma subverts specific host lipids and that its proliferation is limited by the availability of host hemolymph-lipids
Summary
Many insects harbor facultative bacterial endosymbionts, which despite not being required for host survival have important implications for host biology (Wernegreen, 2012). Facultative endosymbionts with strict maternal transmission, including Wolbachia and Spiroplasma, increase their prevalence in host populations by virtue of two strategies: (i) manipulating host reproduction to increase the fitness of infected hosts (Werren and O'Neill, 1997); (ii) inducing a direct increase in host fitness in a manner that is usually condition dependent, for example protecting hosts against different classes of parasites (Hedges et al, 2008; Jaenike et al, 2010; Teixeira et al, 2008). Protective endosymbionts of disease vectors may be useful for the control of vector borne disease, and they are increasingly being studied in this context (Moreira et al, 2009) While these interactions are clearly of importance, more fundamental features of facultative endosymbioses are poorly understood and frequently overlooked, including metabolic exchanges and the mitigation of host fitness costs
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