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Drosophila melanogaster Selection for Survival of Bacillus cereus Infection: Life History Trait Indirect Responses

DOI: 10.1155/2012/935970

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Abstract:

To study evolved resistance/tolerance in an insect model, we carried out an experimental evolution study using D. melanogaster and the opportunistic pathogen B. cereus as the agent of selection. The selected lines evolved a 3.0- to 3.3-log increase in the concentration of spores required for 50% mortality after 18–24 generations of selection. In the absence of any treatment, selected lines evolved an increase in egg production and delayed development time. The latter response could be interpreted as a cost of evolution. Alternatively, delayed development might have been a target of selection resulting in increased adult fat body function including production of antimicrobial peptides, and, incidentally, yolk production for oocytes and eggs. When treated with autoclaved spores, the egg production difference between selected and control lines was abolished, and this response was consistent with the hypothesis of a cost of an induced immune response. Treatment with autoclaved spores also reduced life span in some cases and elicited early-age mortality in the selected and wound-control lines both of which were consistent with the hypothesis of a cost associated with induction of immune responses. In general, assays on egg production yielded key outcomes including the negative effect of autoclaved spores on egg production. 1. Introduction Genetic selection in the laboratory provides a powerful tool for evolutionary analysis of complex traits [1]. It has been used to study many phenomena at different levels of biological organization including life histories, physiology, demography and population dynamics, behavior, form, sex, whole-genome evolution, altruism, and speciation [2]. Selection results in amplification of genetic differences between selected and control lines which is the basis of phenotypic differentiation. Often, correlated (indirect) responses to selection are of particular interest in these experiments as they can suggest tradeoffs between traits. For example, selection for increased D. melanogaster life span and late-age reproduction resulted in decreased early-age reproduction [3, 4]. The nature of tradeoffs between traits is an important topic in life history evolution [5]. In the present study, the insect model D. melanogaster has been used in selection experiments for increased survival after bacterial infection. A previous study of responses in a laboratory selection experiment using Pseudomonas aeruginosa has examined the impact of D. melanogaster resistance on life history traits [6]. This study showed considerable costs in life span

References

[1]  R. B. Huey and F. Rosenzweig, “Laboratory evolution meets catch-22, balancing simplicity and realism,” in Experimental Evolution, T. Garland and M. R. Rose, Eds., University of California Press, 2009.
[2]  T. Garland Jr. and S. A. Kelly, “Phenotypic plasticity and experimental evolution,” Journal of Experimental Biology, vol. 209, no. 12, pp. 2344–2361, 2006.
[3]  M. R. Rose, “Laboratory evolution of postponed senescence in Drosophila melanogaster,” Evolution, vol. 38, pp. 1004–1010, 1984.
[4]  L. S. Luckinbill, R. Arking, M. J. Clare, W. C. Cirocco, and S. A. Buck, “Selection for delayed senescence in Drosophila melanogaster,” Evolution, vol. 38, pp. 996–1003, 1984.
[5]  A. J. Zera and L. G. Harshman, “The physiology of life history trade-offs in animals,” Annual Review of Ecology and Systematics, vol. 32, pp. 95–126, 2001.
[6]  Y. H. Ye, S. F. Chenoweth, and E. A. McGraw, “Effective but costly, evolved mechanisms of defense against a virulent opportunistic pathogen in Drosophila melanogaster,” PLoS Pathogens, vol. 5, no. 4, Article ID e1000385, 2009.
[7]  A. R. Kraaijeveld and H. C. J. Godfrey, “Trade-off between parasitoid resistance and larval competitive ability in Drosophila melanogaster,” Nature, vol. 389, no. 6648, pp. 278–280, 1997.
[8]  M. D. E. Fellowes, A. R. Kraaijeveld, and H. C. J. Godfray, “Trade-off associated with selection for increased ability to resist parasitoid attack in Drosophila melanogaster,” Proceedings of the Royal Society B, vol. 265, no. 1405, pp. 1553–1558, 1998.
[9]  A. R. Kraaijeveld, E. C. Limentani, and H. C. J. Godfray, “Basis of the trade-off between parasitoid resistance and larval competitive ability in Drosophila melanogaster,” Proceedings of the Royal Society B, vol. 268, no. 1464, pp. 259–261, 2001.
[10]  A. R. Kraaijeveld, J. Ferrari, and H. C. J. Godfray, “Costs of resistance in insect-parasite and insect-parasitoid interactions,” Parasitology, vol. 125, pp. S71–S82, 2002.
[11]  M. Lipsitch and A. O. Sousa, “Historical intensity of natural selection for resistance to tuberculosis,” Genetics, vol. 161, no. 4, pp. 1599–1607, 2002.
[12]  D. P. Kwiatkowski, “How malaria has affected the human genome and what human genetics can teach us about malaria,” American Journal of Human Genetics, vol. 77, no. 2, pp. 171–192, 2005.
[13]  M. E. Westhusin, T. Shin, J. W. Templeton, R. C. Burghardt, and L. G. Adams, “Rescuing valuable genomes by animal cloning: a case for natural disease resistance in cattle,” Journal of Animal Science, vol. 85, no. 1, pp. 138–142, 2007.
[14]  E. M. Ibeagha-Awemu, P. Kgwatalala, A. E. Ibeagha, and X. Zhao, “A critical analysis of disease-associated DNA polymorphisms in the genes of cattle, goat, sheep, and pig,” Mammalian Genome, vol. 19, no. 4, pp. 226–245, 2008.
[15]  D. C. Ko, K. P. Shukla, C. Fong et al., “A genome-wide in vitro bacterial-infection screen reveals human variation in the host response associated with inflammatory disease,” American Journal of Human Genetics, vol. 85, no. 2, pp. 214–227, 2009.
[16]  F. Calenge, P. Kaiser, A. Vignal, and C. Beaumont, “Genetic control of resistance to salmonellosis and to Salmonella carrier-state in fowl: a review,” Genetics, Selection, Evolution, vol. 42, article 11, 2010.
[17]  T. E. Schwasinger-Schmidt, S. D. Kachman, and L. G. Harshman, “Evolution of starvation resistance in Drosophila melanogaster: measurement of direct and correlated responses to artificial selection,” Journal of Evolutionary Biology, vol. 25, pp. 378–387, 2012.
[18]  W. Nicholson and P. Setlow, “Sporulation, germination and outgrowth,” in Molecular Biological Methods for Bacillus, C. R. Harwood and S. M. Cutting, Eds., John Wiley and Sons, 1990.
[19]  K. A. McKean and B. P. Lazzaro, “The costs of immunity and the evolution of immunological defense mechanisms,” in Mechanisms of Life History Evolution, T. Flatt and A. Heyland, Eds., Oxford University Press, 2011.
[20]  C. A. Anderson, G. Boucher, C. W. Lees, et al., “Meta-analysis identifies 29 additional ulcerative colitis risk loci, increasing the number of confirmed associations to 47,” Nature Genetics, vol. 43, pp. 246–252, 2011.
[21]  I. F. Goldman, J. Arnold, and B. C. Carlton, “Selection for resistance to Bacillus thuringiensis subspecies israelensis in field and laboratory populations of the mosquito Aedes aegypti,” Journal of Invertebrate Pathology, vol. 47, no. 3, pp. 317–324, 1986.
[22]  B. Tabashnick, “Evolution of resistance to Bacillus thuringiensis,” Annual Review of Entomology, vol. 39, pp. 47–79, 1994.
[23]  L. G. Harshman and A. J. Zera, “The cost of reproduction: the devil in the details,” Trends in Ecology and Evolution, vol. 22, no. 2, pp. 80–86, 2007.
[24]  K. M. Fedorka, M. Zuk, and T. A. Mousseau, “Immune suppression and the cost of reproduction in the ground cricket, Allonemobius socius,” Evolution, vol. 58, no. 11, pp. 2478–2485, 2004.
[25]  K. A. McKean and L. Nunney, “Bateman's principle and immunity: phenotypically plastic reproductive strategies predict changes in immunological sex differences,” Evolution, vol. 59, no. 7, pp. 1510–1517, 2005.
[26]  T. Flatt, K.-J. Min, C. D'Alterio et al., “Drosophila germ-line modulation of insulin signaling and lifespan,” Proceedings of the National Academy of Sciences of the United States of America, vol. 105, no. 17, pp. 6368–6373, 2008.
[27]  F. W. Avila, K. R. Ram, M. C. Bloch Qazi, and M. F. Wolfner, “Sex peptide is required for the efficient release of stored sperm in mated Drosophila females,” Genetics, vol. 186, no. 2, pp. 595–600, 2010.
[28]  E. Kubli, “Sex-peptides: seminal peptides of the Drosophila male,” Cellular and Molecular Life Sciences, vol. 60, no. 8, pp. 1689–1704, 2003.
[29]  D. J. Clancy, D. Gems, L. G. Harshman et al., “Extension of life-span by loss of CHICO, a Drosophila insulin receptor substrate protein,” Science, vol. 292, no. 5514, pp. 104–106, 2001.
[30]  M. Tatar, A. Kopelman, D. Epstein, M. P. Tu, C. M. Yin, and R. S. Garofalo, “A mutant Drosophila insulin receptor homolog that extends life-span and impairs neuroendocrine function,” Science, vol. 292, no. 5514, pp. 107–110, 2001.
[31]  D. S. Richard, R. Rybczynski, T. G. Wilson et al., “Insulin signaling is necessary for vitellogenesis in Drosophila melanogaster independent of the roles of juvenile hormone and ecdysteroids: female sterility of the chico1 insulin signaling mutation is autonomous to the ovary,” Journal of Insect Physiology, vol. 51, no. 4, pp. 455–464, 2005.
[32]  D. Drummond-Barbosa and A. C. Spradling, “Stem cells and their progeny respond to nutritional changes during Drosophila oogenesis,” Developmental Biology, vol. 231, no. 1, pp. 265–278, 2001.
[33]  J. R. DiAngelo, M. L. Bland, S. Bambina, S. Cherry, and M. J. Birnbaum, “The immune response attenuates growth and nutrient storage in Drosophila by reducing insulin signaling,” Proceedings of the National Academy of Sciences of the United States of America, vol. 106, no. 49, pp. 20853–20858, 2009.
[34]  A. K. Chippindale, J. A. Alipaz, H.-W. Chen, and M. R. Rose, “Experimental evolution of accelerated development in Drosophila. 1. Developmental speed and larval survival,” Evolution, vol. 51, no. 5, pp. 1536–1551, 1997.
[35]  N. G. Prasad, M. Shakarad, D. Anitha, M. Rajamani, and A. Joshi, “Correlated responses to selection for faster development and early reproduction in Drosophila: the evolution of larval traits,” Evolution, vol. 55, no. 7, pp. 1363–1372, 2001.
[36]  L. G. Harshman, J. A. Ottea, and B. D. Hammock, “Evolved environment-dependent expression of detoxication enzyme activity in Drosophila melanogaster,” Evolution, vol. 45, pp. 791–795, 1991.
[37]  T. Garland Jr. and S. A. Kelly, “Phenotypic plasticity and experimental evolution,” Journal of Experimental Biology, vol. 209, no. 12, pp. 2344–2361, 2006.

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