细菌感染对黑腹果蝇雌性繁殖力的非同步影响

IF 2.2 Q1 ENTOMOLOGY
Aabeer Basu, Vandana Gupta , Kimaya Tekade , Nagaraj Guru Prasad
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引用次数: 0

摘要

现有理论对病原体感染对宿主繁殖能力的影响做出了不同的预测。终端投资理论认为,由于死亡风险增加,以及与之相关的失去未来繁殖机会的风险,受感染的个体会增加对繁殖的投资。生命史理论认为,由于进行免疫防御需要耗费能量和资源,宿主会减少对繁殖的投资,将资源重新分配用于防御和生存。此外,宿主因感染而造成的体细胞损伤预计也会损害宿主的繁殖能力。我们在实验感染了致病细菌的雌性黑腹果蝇身上探索了这些可能性。我们测试了感染对雌果蝇繁殖力的影响是否具有病原体特异性,是否由感染结果决定,以及感染雌果蝇个体之间是否存在差异。我们观察到,感染后雌性繁殖力在种群水平上的平均变化具有病原体特异性,但与死亡风险无关。此外,感染结果,即受感染雌性死亡还是存活,在这一水平上对繁殖力没有影响。在个体分辨率上,与感染后存活的雌性相比,感染后死亡的雌性在繁殖力上表现出更大的差异。这种增大的变化是双向的,与对照组相比,一些雌性繁殖过多,而另一些则繁殖较少。总之,我们的研究结果表明,感染后雌性繁殖力不太可能受死亡风险的驱动,而可能是由受感染雌性在感染特定病原体时所经历的精确生理变化决定的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Idiosyncratic effects of bacterial infection on female fecundity in Drosophila melanogaster
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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来源期刊
Current Research in Insect Science
Current Research in Insect Science Agricultural and Biological Sciences-Animal Science and Zoology
CiteScore
3.20
自引率
0.00%
发文量
22
审稿时长
36 days
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