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Review
. 2014 Jan;42(1):111-23.
doi: 10.1016/j.dci.2013.06.001. Epub 2013 Jun 10.

Insights from natural host-parasite interactions: the Drosophila model

Affiliations
Review

Insights from natural host-parasite interactions: the Drosophila model

Erin S Keebaugh et al. Dev Comp Immunol. 2014 Jan.

Abstract

Immune responses against opportunistic pathogens have been extensively studied in Drosophila, leading to a detailed map of the genetics behind innate immunity networks including the Toll, Imd, Jak-Stat, and JNK pathways. However, immune mechanisms of other organisms, such as plants, have primarily been investigated using natural pathogens. It was the use of natural pathogens in plant research that revealed the plant R-Avr system, a specialized immune response derived from antagonistic coevolution between plant immune proteins and their natural pathogens' virulence proteins. Thus, we recommend that researchers begin to use natural Drosophila pathogens to identify novel immune strategies that may have arisen through antagonistic coevolution with common natural pathogens. In this review, we address the benefits of using natural pathogens in research, describe the known natural pathogens of Drosophila, and discuss the future prospects for research on natural pathogens of Drosophila.

Keywords: Coevolution; Drosophila immunity; Natural pathogens.

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Figures

Figure 1
Figure 1
A plant example of host-parasite antagonistic coevolution. In Step A, host plants evolve an anti-parasite immune response that protects them from most parasites. Specialist parasites evolve suppressive virulence mechanisms in Step B, selecting the plant hosts to counter-evolve secondary immune mechanisms in Step C. Steps B and C can then repeatedly cycle in an evolutionary "arms race". Use of non-natural parasites in infection experiments can limit our understanding of host immunity to the general types of immune responses exemplified in Step A. (Chisholm et al., 2006).
Figure 2
Figure 2
Evolution of immune genes in Drosophila simulans. Numerous secreted and hemocyte membrane-bound antigen receptors are represented, as well as members of the Toll and Imd pathways, which control the humoral response to microbial infections in the fat body. Genes shown in blue showed significant evidence of adaptive evolution along the D. simulans lineage. These data suggest that the main virulence strategy of natural D. simulans parasites is production of secreted virulence proteins that suppress immune signaling through the Toll and Imd pathways, rather than recognition avoidance or antimicrobial peptide tolerance (antimicrobial peptide data not shown) (Schlenke and Begun, 2003).
Figure 3
Figure 3
The natural parasites of Drosophila. The parasites are arranged by phylogenetic group as well as by the fruit fly life stage they infect. Note that all parasites that infect fly eggs are transmitted vertically from parent flies, while all other parasites are horizontally transferred. Only parasites specifically named in the text or identified by screens are included. Other natural parasites of Drosophila have been dentified but are relatively uncharacterized and not included here.
Figure 4
Figure 4
Interactions between Drosophila and endoparasitoid wasps. Wasps inject an egg and venom into the body cavity of a fly larva, and the fly recognizes the egg as foreign and mounts a melanotic encapsulation response. However, wasps evolve venom proteins that have specific ways of suppressing this fly immune response.

References

    1. Adams MD, Celniker SE, Holt RA, Evans CA, Gocayne JD, Amanatides PG, Scherer SE, Li PW, Hoskins RA, Galle RF, George RA, Lewis SE, Richards S, Ashburner M, Henderson SN, Sutton GG, Wortman JR, Yandell MD, Zhang Q, Chen LX, Brandon RC, Rogers YH, Blazej RG, Champe M, Pfeiffer BD, Wan KH, Doyle C, Baxter EG, Helt G, Nelson CR, Gabor GL, Abril JF, Agbayani A, An HJ, Andrews-Pfannkoch C, Baldwin D, Ballew RM, Basu A, Baxendale J, Bayraktaroglu L, Beasley EM, Beeson KY, Benos PV, Berman BP, Bhandari D, Bolshakov S, Borkova D, Botchan MR, Bouck J, Brokstein P, Brottier P, Burtis KC, Busam DA, Butler H, Cadieu E, Center A, Chandra I, Cherry JM, Cawley S, Dahlke C, Davenport LB, Davies P, de Pablos B, Delcher A, Deng Z, Mays AD, Dew I, Dietz SM, Dodson K, Doup LE, Downes M, Dugan-Rocha S, Dunkov BC, Dunn P, Durbin KJ, Evangelista CC, Ferraz C, Ferriera S, Fleischmann W, Fosler C, Gabrielian AE, Garg NS, Gelbart WM, Glasser K, Glodek A, Gong F, Gorrell JH, Gu Z, Guan P, Harris M, Harris NL, Harvey D, Heiman TJ, Hernandez JR, Houck J, Hostin D, Houston KA, Howland TJ, Wei MH, Ibegwam C, Jalali M, Kalush F, Karpen GH, Ke Z, Kennison JA, Ketchum KA, Kimmel BE, Kodira CD, Kraft C, Kravitz S, Kulp D, Lai Z, Lasko P, Lei Y, Levitsky AA, Li J, Li Z, Liang Y, Lin X, Liu X, Mattei B, McIntosh TC, McLeod MP, McPherson D, Merkulov G, Milshina NV, Mobarry C, Morris J, Moshrefi A, Mount SM, Moy M, Murphy B, Murphy L, Muzny DM, Nelson DL, Nelson DR, Nelson KA, Nixon K, Nusskern DR, Pacleb JM, Palazzolo M, Pittman GS, Pan S, Pollard J, Puri V, Reese MG, Reinert K, Remington K, Saunders RD, Scheeler F, Shen H, Shue BC, Siden-Kiamos I, Simpson M, Skupski MP, Smith T, Spier E, Spradling AC, Stapleton M, Strong R, Sun E, Svirskas R, Tector C, Turner R, Venter E, Wang AH, Wang X, Wang ZY, Wassarman DA, Weinstock GM, Weissenbach J, Williams SM, Woodage T, Worley KC, Wu D, Yang S, Yao QA, Ye J, Yeh RF, Zaveri JS, Zhan M, Zhang G, Zhao Q, Zheng L, Zheng XH, Zhong FN, Zhong W, Zhou X, Zhu S, Zhu X, Smith HO, Gibbs RA, Myers EW, Rubin GM, Venter JC. The genome sequence of Drosophila melanogaster . Science. 2000;287:2185–2195. - PubMed
    1. Allemand R, Lemaitre C, Frey F, Bouletreau M, Vavre F, Nordlander G, van Alphen J, Carton Y. Phylogeny of six African Leptopilina species (Hymenoptera: Cynipoidea: Figitidae), parasitoids of Drosophila, with description of three new species. Ann Soc Entomol F. 2002;39:319–332.
    1. Aminetzach YT, Macpherson JM, Petrov DA. Pesticide resistance via transposition-mediated adaptive gene truncation in Drosophila. Science. 2005;309:764–767. - PubMed
    1. Anthony RM, Rutitzky LI, Urban JF, Jr, Stadecke MJ, Gause WC. Protective immune mechanisms in helminth infection. Nat Rev Immunol. 2007;7:975–987. - PMC - PubMed
    1. Asai T, Tena G, Plotnikova J, Willmann MR, Chiu WL, Gomez-Gomez L, Boller T, Ausubel FM, Sheen J. MAP kinase signalling cascade in Arabidopsis innate immunity. Nature. 2002;415:977–983. - PubMed

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