“…Insects combat wasp infestation by encapsulation, a cellular immune process that involves the formation of a capsule composed of large flat hemocytes called lamellocytes. Lamellocytes stick around the developing wasp larva and are subsequently melanized by prophenoloxidase from both lamellocytes and crystal cells ( 33 , 35 , 36 ). Lamellocytes differentiate from 0 to 24 h postinfestation from hemocyte progenitors in the lymph gland or directly from plasmatocytes present in the circulation or in the sessile niche ( 37 ).…”
Insects commonly harbor facultative bacterial endosymbionts, such as Wolbachia and Spiroplasma species, that are vertically transmitted from mothers to their offspring. These endosymbiontic bacteria increase their propagation by manipulating host reproduction or by protecting their hosts against natural enemies. While an increasing number of studies have reported endosymbiont-mediated protection, little is known about the mechanisms underlying this protection. Here, we analyze the mechanisms underlying protection from parasitoid wasps in Drosophila melanogaster mediated by its facultative endosymbiont Spiroplasma poulsonii. Our results indicate that S. poulsonii exerts protection against two distantly related wasp species, Leptopilina boulardi and Asobara tabida. S. poulsonii-mediated protection against parasitoid wasps takes place at the pupal stage and is not associated with an increased cellular immune response. In this work, we provide three important observations that support the notion that S. poulsonii bacteria and wasp larvae compete for host lipids and that this competition underlies symbiont-mediated protection. First, lipid quantification shows that both S. poulsonii and parasitoid wasps deplete D. melanogaster hemolymph lipids. Second, the depletion of hemolymphatic lipids using the Lpp RNA interference (Lpp RNAi) construct reduces wasp success in larvae that are not infected with S. poulsonii and blocks S. poulsonii growth. Third, we show that the growth of S. poulsonii bacteria is not affected by the presence of the wasps, indicating that when S. poulsonii is present, larval wasps will develop in a lipid-depleted environment. We propose that competition for host lipids may be relevant to endosymbiont-mediated protection in other systems and could explain the broad spectrum of protection provided.
“…Insects combat wasp infestation by encapsulation, a cellular immune process that involves the formation of a capsule composed of large flat hemocytes called lamellocytes. Lamellocytes stick around the developing wasp larva and are subsequently melanized by prophenoloxidase from both lamellocytes and crystal cells ( 33 , 35 , 36 ). Lamellocytes differentiate from 0 to 24 h postinfestation from hemocyte progenitors in the lymph gland or directly from plasmatocytes present in the circulation or in the sessile niche ( 37 ).…”
Insects commonly harbor facultative bacterial endosymbionts, such as Wolbachia and Spiroplasma species, that are vertically transmitted from mothers to their offspring. These endosymbiontic bacteria increase their propagation by manipulating host reproduction or by protecting their hosts against natural enemies. While an increasing number of studies have reported endosymbiont-mediated protection, little is known about the mechanisms underlying this protection. Here, we analyze the mechanisms underlying protection from parasitoid wasps in Drosophila melanogaster mediated by its facultative endosymbiont Spiroplasma poulsonii. Our results indicate that S. poulsonii exerts protection against two distantly related wasp species, Leptopilina boulardi and Asobara tabida. S. poulsonii-mediated protection against parasitoid wasps takes place at the pupal stage and is not associated with an increased cellular immune response. In this work, we provide three important observations that support the notion that S. poulsonii bacteria and wasp larvae compete for host lipids and that this competition underlies symbiont-mediated protection. First, lipid quantification shows that both S. poulsonii and parasitoid wasps deplete D. melanogaster hemolymph lipids. Second, the depletion of hemolymphatic lipids using the Lpp RNA interference (Lpp RNAi) construct reduces wasp success in larvae that are not infected with S. poulsonii and blocks S. poulsonii growth. Third, we show that the growth of S. poulsonii bacteria is not affected by the presence of the wasps, indicating that when S. poulsonii is present, larval wasps will develop in a lipid-depleted environment. We propose that competition for host lipids may be relevant to endosymbiont-mediated protection in other systems and could explain the broad spectrum of protection provided.
“…L. heterotoma does, however, not perform equally well on all these species, due to differences in suitability, and species-specific immune reactions. Following oviposition of a wasp, a parasitized host can indeed initiate an immune response in <48 h in an attempt to kill the wasp's egg (Mortimer, 2013;Nappi, 1975;Poyet et al, 2013).…”
Section: Hos T Su Itab Ilit Y Hos T Re S Is Tan Ce and Par A S Itoid...mentioning
confidence: 99%
“…in great detail (Mortimer, 2013;Nappi, 2010;Poirié et al, 2009Poirié et al, , 2014Wertheim, 2022;Yang et al, 2020); hence here we emphasize the work done on host suitability, host immunity and L. heterotoma virulence.…”
Section: Hos T Su Itab Ilit Y Hos T Re S Is Tan Ce and Par A S Itoid...mentioning
The parasitoid Leptopilina heterotoma has been used as a model system for more than 70 years, contributing greatly to diverse research areas in ecology and evolution. Here, we synthesized the large body of work on L. heterotoma with the aim to identify new research avenues that could be of interest also for researchers studying other parasitoids and insects. We start our review with a description of typical L. heterotoma characteristics, as well as that of the higher taxonomic groups to which this species belongs. We then continue discussing host suitability and immunity, foraging behaviors, as well as fat accumulation and life histories. We subsequently shift our focus towards parasitoid‐parasitoid interactions, including L. heterotoma coexistence within the larger guild of Drosophila parasitoids, chemical communication, as well as mating and population structuring. We conclude our review by highlighting the assets of L. heterotoma as a model system, including its intermediate life history syndromes, the ease of observing and collecting natural hosts and wasps, as well as recent genomic advances.
“…Parasitoid wasps that infect Drosophila are a valuable model for understanding parasite behavior and have provided important ecological and molecular insights into host–parasite interactions [ 1 , 2 , 3 ]. In this system, parasitoids infect larval Drosophila , and following infection, Drosophila mount a cellular encapsulation response to overcome the invader [ 4 ].…”
The interactions between Drosophila melanogaster and the parasitoid wasps that infect Drosophila species provide an important model for understanding host–parasite relationships. Following parasitoid infection, D. melanogaster larvae mount a response in which immune cells (hemocytes) form a capsule around the wasp egg, which then melanizes, leading to death of the parasitoid. Previous studies have found that host hemocyte load; the number of hemocytes available for the encapsulation response; and the production of lamellocytes, an infection induced hemocyte type, are major determinants of host resistance. Parasitoids have evolved various virulence mechanisms to overcome the immune response of the D. melanogaster host, including both active immune suppression by venom proteins and passive immune evasive mechanisms. We identified a previously undescribed parasitoid species, Asobara sp. AsDen, which utilizes an active virulence mechanism to infect D. melanogaster hosts. Asobara sp. AsDen infection inhibits host hemocyte expression of msn, a member of the JNK signaling pathway, which plays a role in lamellocyte production. Asobara sp. AsDen infection restricts the production of lamellocytes as assayed by hemocyte cell morphology and altered msn expression. Our findings suggest that Asobara sp. AsDen infection alters host signaling to suppress immunity.
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