Géraldine Doury

Resistance of Drosophila suzukii to the larval parasitoids Leptopilina heterotoma and Asobara japonica is related to haemocyte load.

Unlike other Drosophila species, the invasive Drosophila suzukii Matsumura (Diptera: Drosophilidae) shows a remarkable pest status. Among the physiological traits that may explain the high level of resistance to parasitoids of Drosophila larvae, the haemocyte load is shown repeatedly to play an important role. To determine whether haemocyte load can explain immunity resistance of D. suzukii to parasitoids, the haemocytes of parasitized and healthy larvae are quantified in two Japanese and three French populations of D. suzukii. Parasitization tests are conducted with two larval parasitoids: the paleartic Leptopilina heterotoma Thomson (Hymenoptera: Figitidae) and the Asian Asobara japonica Belokobylskij (Hymenoptera: Braconidae). Based on morphological and functional criteria, D. suzukii has classes of haemocytes similar to those described in Drosophila melanogaster. However, healthy larvae of the five populations tested possess particularly large numbers of haemocytes compared with D. melanogaster. Haemocyte load is also higher in larvae from the French populations than in the Japanese strains. The ability of D. suzukii larvae to encapsulate eggs of L. heterotoma is associated with a particularly high load of circulating haemocytes. However, it is notable that A. japonica induces a strong depression of the haemocyte population in this resistant host associated with an inability to encapsulate parasitoid eggs. The results show that the cellular immune system plays a major role in the failure of larval parasitoids to develop in most instances in larvae of D. suzukii, possibly contributing to the success of this species as an invader.

Comparative study of the strategies evolved by two parasitoids of the genus Asobara to avoid the immune response of the host, Drosophila melanogaster

Asobara tabida and Asobara citri are two braconid endoparasitoids of Drosophila melanogaster larvae. We studied and compared the strategies evolved by these two species to avoid the immune reaction of their host. A. tabida has no negative impact on host cellular defenses and its eggs avoid encapsulation by adhering to host tissues. At the opposite, we found that A. citri, whose eggs are devoid of adhesive properties, affects the host encapsulation abilities, hemolymph phenoloxidase activity and concentrations of circulating hemocytes. Some of these effects could directly rely on a severe disruption of the hematopoietic organ anterior lobes observed in parasitized larvae. This is the first report of the immune suppressive abilities of a parasitoid from the Asobara genus. Results are presented and discussed with respect to the strategies of virulence evolved by other parasitoids to counteract the D. melanogaster immune system.

Effects of parasitism by Asobara tabida (Hymenoptera: Braconidae) on the development, survival and activity of Drosophila melanogaster larvae.

The impact of parasitism by Asobara tabida on Drosophila melanogaster larval development, survival features and larval activity has been investigated using two strains of the parasitoid. The successful parasitism rate of the A1 strain was four times greater than that of the WOPV strain. Both strains induced equivalent mortality rates but hosts parasitized by A1 predominantly died as pupae. The time necessary for the host pupariation and emergence, and the larval weight at 72, 96 and 120 h post-parasitization were measured. Parasitized larvae exhibited longer periods of development and lower weights than controls, especially when parasitized by A1. These results suggest that hosts underwent physiological costs varying with respect to the outcome of the parasitic relationship. Of the parasitoid factors possibly responsible for these costs, we examined venoms for their impact on host mortality. Artificial injections of WOPV venoms induced higher mortality rates than did A1 venoms. Venoms were also found responsible for the induction of a transient paralysis, naturally occuring after parasitization. Again, the strongest effect was observed after parasitization by WOPV or injections of its venoms. This study gives new insights into the intriguing features of A. tabida and constitutes the first report of the paralysing properties of the venoms.

Deadly venom of Asobara japonica parasitoid needs ovarian antidote to regulate host physiology.

Asobara japonica (Braconidae) is an endophagous parasitoid developing in Drosophila larvae. The present study shows that A. japonica was never encapsulated in Drosophila melanogaster, and that it caused an overall inhibition of the host encapsulation reaction since injected foreign bodies were never encapsulated in parasitized hosts. Both the number of circulating hemocytes and the phenoloxidase activity decreased in parasitized larvae, and the hematopoietic organ appeared highly disrupted. We also found that A. japonica venom secretions had atypical effects on hosts compared to other braconid wasps. A. japonica venom secretions induced permanent paralysis followed by death of D. melanogaster larvae, whether injected by the female wasp during an interrupted oviposition, or manually injected into unparasitized larvae. More remarkably, these effects could be reversed by injection of ovarian extracts from female wasps. This is the first report that the venom of an endophagous braconid parasitoid can have a deadly effect on hosts, and moreover, that ovarian extracts can act as an antidote to reverse the effects of the wasps venom. These results also demonstrate that A. japonica secretions from both venom gland and ovary are required to regulate synergistically the host physiology for the success of the parasitoid.

Immune Resistance of Drosophila Hosts Against Asobara Parasitoids: Cellular Aspects

The immunity of Drosophila relies on a variety of defenses cooperating to fight parasites and pathogens. The encapsulation reaction is the main hemocytic response neutralizing large parasites like endophagous parasitoids. The diversity of the mechanisms of immunoevasion evolved by Asobara parasitoids, together with the wide spectrum of Drosophila host species they can parasitize, make them ideal models to study and unravel the physiological and cellular aspects of host immunity. This chapter summarizes what could be learnt on the cellular features of the encapsulation process in various Drosophila spp., and also on the major role played by Drosophila hosts hemocytes subpopulations, both in a quantitative and qualitative manner, regarding the issue of the immune Asobara-Drosophila interactions.

Trans-Generational Effects of Mild Heat Stress on the Life History Traits of an Aphid Parasitoid

Temperature changes are common in nature and insects are particularly exposed and sensitive to such variations which can be potential stresses, ultimately affecting life history traits and overall fitness. Braconids have been widely used to study the effects of temperature on host-parasitoid interactions and the present work focused on the solitary endoparasitoid Aphidius ervi Haliday (Hymenoptera: Braconidae Aphidiidae), an efficient biological control agent commercially used against aphids such as the potato aphid Macrosiphum euphorbiae Thomas (Sternorrhyncha: Aphididae). Contrary to previous studies using heat shocks at extreme temperatures, we evaluated the effects of mild heat stresses by transferring young parasitoid adults from the constant temperature of 20°C to either a warm (25°C) or hot (28°C) temperature, for either 1 h or 48 h. Such treatments are consistent with situations commonly experienced by parasitoids when moved from their rearing conditions to greenhouses or field conditions. The effects were evaluated both on the heat stressed A. ervi adults (G0) (immediate effects) and on their first generation (G1) progeny (trans-generational effects). G0 wasps’ mortality was significantly affected by the temperature in interaction with the duration of the stress. Longevity of G0 wasps surviving the heat stress was negatively affected by the temperature and females lived longer than males. Heat stress applied to A. ervi parents also had consequences on their G1 progeny whose developmental time, rates of mummification and percentage of parasitoid completing total development were negatively affected. Surprisingly, the egg load at emergence of the G1 female progeny was increased when their mothers had been submitted to a mild heat stress of 25°C or 28°C. These results clearly demonstrate trans-generational phenotypic plasticity, showing that adaptation to thermal stresses may be achieved via maternal effects. This study also sheds light on the complexity of insect responses and underlying mechanisms to fluctuating conditions in their natural environment.

When Parasitoids Lack Polydnaviruses, Can Venoms Subdue the Hosts? The Case Study of Asobara Species

Host regulation has been described as the many effects-- mostly physiological changes--that parasitoids cause in their host which benefit their own development (Vinson and Iwantsch, 1980). It evokes developmental disruption usually via hormonal or neurohormonal pathways, like the endocrine signaling which coordinates development of the parasitoid with that of the host so that the two partners molt in synchrony (Beckage and Gelman, 2004). It also includes all the effects on the host immune system (Strand and Pech, 1995; Schmidt et al., 2001; Pennacchio and Strand, 2006; Carton et al., 2008; Eslin et al., 2009), the first physiological barrier that endophagous parasitoids encounter after they enter the hemocoel of their host. In order to regulate their hosts immunity and physiology, parasitoids produce and release active factors in the host hemocoel. These factors may come from either the female wasps reproductive apparatus and its associated glands, or the parasitic egg or larva itself. In many species of the ichneumonid and braconid families (Ichneumonoidea), symbiotic polydnaviruses (PDVs) or virus-like particles (VLPs) (Schmidt and Schumann-Feddersen, 1989; Strand and Pech, 1995; Beckage, 1998; Drezen et al., 2003; Beckage and Gelman, 2004; Pennacchio and Strand, 2006; Bezier et al., 2009) can act as infecting agents. PDVs multiply in the calyx cells of the female wasps ovaries while