Idiosyncratic effects of bacterial infection on female fecundity in Drosophila melanogaster

被引:0
|
作者
Basu, Aabeer [1 ]
Gupta, Vandana [1 ,2 ]
Tekade, Kimaya [1 ,3 ]
Prasad, Nagaraj Guru [1 ]
机构
[1] Indian Inst Sci Educ & Res Mohali, Dept Biol Sci, Sect 81, SAS Nagar 140306, Punjab, India
[2] Univ Montpellier, Inst Evolutionary Sci, Pl Eugene Bataillon, F-34095 Montpellier 05, France
[3] Univ Regensburg, Univ Hosp Regensburg, Inst Immune Med, Franz Josef Str Allee 11, D-93053 Regensburg, Germany
来源
关键词
Terminal investment; Life-history theory; Cost of immunity; Fecundity compensation; Pathogenic bacterial infection; Inter-individual variation; GENETIC-VARIATION; IMMUNE DEFENSE; TRADE-OFFS; RESISTANCE; FITNESS; TOLERANCE; IMMUNOLOGY; STRATEGIES; REDUCTION; DISEASES;
D O I
10.1016/j.cris.2024.100098
中图分类号
Q96 [昆虫学];
学科分类号
摘要
Existing theories make different predictions regarding the effect of a pathogenic infection on the host capacity to reproduce. Terminal investment theory suggests that due to the increased risk of mortality, and the associated risk of losing future opportunity to reproduce, infected individuals would increase their investment towards reproduction. Life-history theory posits that due to energetic and resource costs associated with mounting an immune defense, hosts would decrease their investment towards reproduction, and reallocate resources towards defense and survival. Additionally, Somatic damage incurred by the host due to the infection is also expected to compromise the host capacity to reproduce. We explored these possibilities in Drosophila melanogaster females experimentally infected with pathogenic bacteria. We tested if the effect of infection on female fecundity is pathogen specific, determined by infection outcome, and variable between individual infected females. We observed that the mean, population level change in post-infection female fecundity was pathogen specific, but not correlated with mortality risk. Furthermore, infection outcome, i.e., if the infected female died or survived the infection, had no effect on fecundity at this level. At individual resolution, females that died after infection exhibited greater variation in fecundity compared to ones that survived the infection. This increased variation was bidirectional, with some females reproducing in excess while others reproducing less compared to the controls. Altogether, our results suggest that post-infection female fecundity is unlikely to be driven by risk of mortality and is probably determined by the precise physiological changes that an infected female undergoes when infected by a specific pathogen.
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页数:8
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