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- Wolbachia and host intrinsic reproductive barriers contribute additively to postmating isolation in spider mitesPublication . Cruz, Miguel; Magalhães, sara; Sucena, Élio; Zélé, FloreWolbachia are maternally-inherited bacteria that induce cytoplasmic incompatibility in many arthropod species. However, the ubiquity of this isolation mechanism for host speciation processes remains elusive, as only few studies have examined Wolbachia-induced incompatibilities when host populations are not genetically compatible. Here, we used three populations of two genetically differentiated colour forms of the haplodiploid spider mite Tetranychus urticae to dissect the interaction between Wolbachia-induced and host-associated incompatibilities, and their relative contribution to postmating isolation. We found that these two sources of incompatibility act through different mechanisms in an additive fashion. Host-associated incompatibility contributes 1.5 times more than Wolbachia-induced incompatibility in reducing hybrid production, the former through an overproduction of haploid sons at the expense of diploid daughters (ca. 75% decrease) and the latter by increasing the embryonic mortality of daughters (by ca. 49%). Furthermore, regardless of cross direction, we observed near-complete F1 hybrid sterility and complete F2 hybrid breakdown between populations of the two forms, but Wolbachia did not contribute to this outcome. We thus show mechanistic independence and an additive nature of host-intrinsic and Wolbachia-induced sources of isolation. Wolbachia may contribute to reproductive isolation in this system, thereby potentially affecting host differentiation and distribution in the field.
- Transdifferentiation of plasmatocytes to crystal cells in the lymph gland of Drosophila melanogasterPublication . Marcetteau, Julien; Duarte, Patrícia; Leitão, Alexandre B; Sucena, ÉlioUnder homeostatic conditions, haematopoiesis in Drosophila larvae occurs in the lymph gland and sessile haemocyte clusters to produce two functionally and morphologically different cells: plasmatocytes and crystal cells. It is well-established that in the lymph gland both cell types stem from a binary decision of the medullary prohaemocyte precursors. However, in sessile clusters and dorsal vessel, crystal cells have been shown to originate from the transdifferentiation of plasmatocytes in a Notch/Serrate-dependent manner. We show that transdifferentiation occurs also in the lymph gland. In vivo phagocytosis assays confirm that cortical plasmatocytes are functionally differentiated phagocytic cells. We uncover a double-positive population in the cortical zone that lineage-tracing and long-term live imaging experiments show will differentiate into crystal cells. The reduction of Notch levels within the lymph gland plasmatocyte population reduces crystal cell number. This extension of a transdifferentiation mechanism reinforces the growing role of haematopoietic plasticity in maintaining homeostasis in Drosophila and vertebrate systems. Future work should test the regulation and relative contribution of these two processes under different immunological and/or metabolic conditions.
- Evolution of resistance and disease tolerance mechanisms to oral bacterial infection in Drosophila melanogasterPublication . Paulo, Tânia F.; Akyaw, Priscilla A.; Paixão, Tiago; Sucena, ÉlioPathogens exert strong selection on hosts that evolve and deploy different defensive strategies, namely minimizing pathogen exposure (avoidance), directly promoting pathogen elimination (resistance) and/or managing the deleterious effects of illness (disease tolerance). However, how the host response partitions across these processes has not been directly tested in a single host–pathogen system, let alone in the context of known adaptive trajectories resulting from experimental evolution. Here, we compare a Drosophila melanogaster population adapted to oral infection with its natural pathogen Pseudomonas entomophila (BactOral), to its control population to find no evidence for behavioural changes but measurable differences in both resistance and disease tolerance. In BactOral, no differences were detected in bacterial intake or defecation, nor gut cell renewal. However, a measurable relative decrease in bacterial loads correlates with an increase in gut-specific anti-microbial peptide production, pointing to a strengthening in resistance. Additionally, we posit that disease tolerance also contributes to the response of BactOral through a tighter control of self- and pathogen-derived damage caused by bacteria exposure. This study reveals a genetically complex and mechanistically multi-layered response, possibly reflecting the structure of adaptation to infection in natural populations.