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Germline regulates the expression of life‐history traits and mediates the trade‐off between reproduction and somatic maintenance. However, germline maintenance in itself can be costly, and the costs can vary between the sexes depending on the number of gametes produced across the lifetime. We tested this directly by germline ablation using glp‐1 RNA interference (RNAi) in a dioecious nematode Caenorhabditis remanei. Germline removal strongly increased heat‐shock resistance in both sexes, thus confirming the role of the germline in regulating somatic maintenance. However, germline removal resulted in increased lifespan only in males. High costs of mating strongly reduced lifespan in both sexes and obliterated the survival benefit of germline‐less males even though neither sex produced any offspring. Furthermore, germline removal reduced male growth before maturation but not in adulthood, while female growth rate was reduced both before and especially after maturation. Thus, germline removal improves male lifespan without major growth costs, while germline‐less females grow slower and do not live longer than reproductively functional counterparts in the absence of environmental stress. Overall, these results suggest that germline maintenance is costlier for males than for females in C. remanei. [ABSTRACT FROM AUTHOR]

Why and how we age are 2 intertwined questions that have fascinated scientists for many decades. However, attempts to answer these questions remain compartmentalized, preventing a comprehensive understanding of the aging process. We argue that the current lack of knowledge about the evolution of aging mechanisms is due to a lack of clarity regarding evolutionary theories of aging that explicitly involve physiological processes: the disposable soma theory (DST) and the developmental theory of aging (DTA). In this Essay, we propose a new hierarchical model linking genes to vital rates, enabling us to critically reevaluate the DST and DTA in terms of their relationship to evolutionary genetic theories of aging (mutation accumulation (MA) and antagonistic pleiotropy (AP)). We also demonstrate how these 2 theories can be incorporated in a unified hierarchical framework. The new framework will help to generate testable hypotheses of how the hallmarks of aging are shaped by natural selection. Why and how we age are two intertwined questions that have fascinated scientists for many decades. This Essay proposes a new hierarchical model that links genes to vital rates, enabling a critical re-evaluation of the disposable soma theory and the developmental theory of aging in terms of their relationship to evolutionary genetic theories of aging. [ABSTRACT FROM AUTHOR]

Males and females rarely express the same length of life. Here, we studied how sociosexual exposure shapes male and female age-specific mortality rates in Drosophila melanogaster. We maintained focal females and males within large, replicated cohorts throughout life with individuals of the same or opposite sex. Consistent with previous works, we found that females kept throughout their lives with males had only half the lifespan of those maintained throughout life at the same density in same-sex cohorts. In contrast, only a small lifespan decrease was observed in the corresponding male treatments and the reduction in male lifespan following exposure throughout life to other males or females was similar. Deconvolution of underlying aging parameters revealed that changes in lifespan were underpinned by opposing effects on actuarial aging in males versus females. Exposure to the opposite or same sex increased initial mortality rate in both sexes. However, in females, increasing exposure to males increased the rate of aging, while increasing exposure to females actually decreased it. The effects were in the opposite direction in males and were much smaller in magnitude. Overall, the findings were consistent with reports suggesting that exposure to the same versus opposite sex can affect survival differently in males and females. However, they also reveal a new insight—that overall lifespan can be underpinned by key differences in actuarial senescence in each sex. The findings suggest that responses to same or opposite sex exposure may have fundamentally and qualitatively different physiological consequences for health in males and females. [ABSTRACT FROM AUTHOR]