{"acknowledgement":"We would like to thank Susann Wicke for performing the genome-wide SNP/indel analyses, as well as Veronica Alves, Kevin Ferro, Momir Futo, Barbara Hasert, Dafne Maximo, Nora Schulz, Marlene Sroka, and Barth Wieczorek for technical help. We thank Brian Lazzaro for the L. lactis strain and Bruno Lemaitre for the Pseudomonas entomophila strain. We would like to thank two anonymous reviewers for their helpful comments. We are grateful to the Deutsche Forschungsgemeinschaft (DFG) priority programme 1399 ‘Host parasite coevolution’ for funding this project (AR 872/1-1). ","isi":1,"intvolume":"        31","publist_id":"7187","volume":31,"year":"2018","citation":{"mla":"Kutzer, Megan, et al. “Genotype and Diet Affect Resistance, Survival, and Fecundity but Not Fecundity Tolerance.” <i>Journal of Evolutionary Biology</i>, vol. 31, no. 1, Wiley, 2018, pp. 159–71, doi:<a href=\"https://doi.org/10.1111/jeb.13211\">10.1111/jeb.13211</a>.","ieee":"M. Kutzer, J. Kurtz, and S. Armitage, “Genotype and diet affect resistance, survival, and fecundity but not fecundity tolerance,” <i>Journal of Evolutionary Biology</i>, vol. 31, no. 1. Wiley, pp. 159–171, 2018.","chicago":"Kutzer, Megan, Joachim Kurtz, and Sophie Armitage. “Genotype and Diet Affect Resistance, Survival, and Fecundity but Not Fecundity Tolerance.” <i>Journal of Evolutionary Biology</i>. Wiley, 2018. <a href=\"https://doi.org/10.1111/jeb.13211\">https://doi.org/10.1111/jeb.13211</a>.","apa":"Kutzer, M., Kurtz, J., &#38; Armitage, S. (2018). Genotype and diet affect resistance, survival, and fecundity but not fecundity tolerance. <i>Journal of Evolutionary Biology</i>. Wiley. <a href=\"https://doi.org/10.1111/jeb.13211\">https://doi.org/10.1111/jeb.13211</a>","ista":"Kutzer M, Kurtz J, Armitage S. 2018. Genotype and diet affect resistance, survival, and fecundity but not fecundity tolerance. Journal of Evolutionary Biology. 31(1), 159–171.","ama":"Kutzer M, Kurtz J, Armitage S. Genotype and diet affect resistance, survival, and fecundity but not fecundity tolerance. <i>Journal of Evolutionary Biology</i>. 2018;31(1):159-171. doi:<a href=\"https://doi.org/10.1111/jeb.13211\">10.1111/jeb.13211</a>","short":"M. Kutzer, J. Kurtz, S. Armitage, Journal of Evolutionary Biology 31 (2018) 159–171."},"article_type":"original","_id":"617","language":[{"iso":"eng"}],"publication":"Journal of Evolutionary Biology","author":[{"id":"29D0B332-F248-11E8-B48F-1D18A9856A87","full_name":"Kutzer, Megan","first_name":"Megan","last_name":"Kutzer","orcid":"0000-0002-8696-6978"},{"full_name":"Kurtz, Joachim","last_name":"Kurtz","first_name":"Joachim"},{"full_name":"Armitage, Sophie","last_name":"Armitage","first_name":"Sophie"}],"doi":"10.1111/jeb.13211","page":"159  - 171","external_id":{"isi":["000419307000014"],"pmid":["29150962"]},"publication_identifier":{"eissn":["1420-9101"],"issn":["1010-061X"]},"title":"Genotype and diet affect resistance, survival, and fecundity but not fecundity tolerance","quality_controlled":"1","status":"public","oa_version":"Published Version","oa":1,"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","date_created":"2018-12-11T11:47:31Z","publisher":"Wiley","scopus_import":"1","date_published":"2018-01-01T00:00:00Z","publication_status":"published","issue":"1","department":[{"_id":"SyCr"}],"main_file_link":[{"url":"https://doi.org/10.1111/jeb.13211","open_access":"1"}],"abstract":[{"lang":"eng","text":"Insects are exposed to a variety of potential pathogens in their environment, many of which can severely impact fitness and health. Consequently, hosts have evolved resistance and tolerance strategies to suppress or cope with infections. Hosts utilizing resistance improve fitness by clearing or reducing pathogen loads, and hosts utilizing tolerance reduce harmful fitness effects per pathogen load. To understand variation in, and selective pressures on, resistance and tolerance, we asked to what degree they are shaped by host genetic background, whether plasticity in these responses depends upon dietary environment, and whether there are interactions between these two factors. Females from ten wild-type Drosophila melanogaster genotypes were kept on high- or low-protein (yeast) diets and infected with one of two opportunistic bacterial pathogens, Lactococcus lactis or Pseudomonas entomophila. We measured host resistance as the inverse of bacterial load in the early infection phase. The relationship (slope) between fly fecundity and individual-level bacteria load provided our fecundity tolerance measure. Genotype and dietary yeast determined host fecundity and strongly affected survival after infection with pathogenic P. entomophila. There was considerable genetic variation in host resistance, a commonly found phenomenon resulting from for example varying resistance costs or frequency-dependent selection. Despite this variation and the reproductive cost of higher P. entomophila loads, fecundity tolerance did not vary across genotypes. The absence of genetic variation in tolerance may suggest that at this early infection stage, fecundity tolerance is fixed or that any evolved tolerance mechanisms are not expressed under these infection conditions."}],"type":"journal_article","day":"01","month":"01","article_processing_charge":"No","date_updated":"2023-09-11T14:06:04Z","pmid":1}