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To distinguish between these models, we manipulated levels of progeny production by controlling sperm availability.
Two basic models can explain the positive correlation between high levels of progeny production and delayed somatic aging: (1) progeny production causes health-span extension or (2) a common cause mediates high levels of progeny production and health span extension.
Increased levels of progeny production did not accelerate somatic aging, indicating that reproductive activity does not cause somatic aging.
However, this analysis indicated that the virus-induced increases in cytokine levels were sustained even in the absence of significant levels of progeny virus production.
To determine the effects of progeny production on somatic aging, we analyzed hermaphrodites with the identical genotype and different levels of progeny production.
The percentage of suppression was calculated as difference between the optical density levels of progeny with and without the heterochromatic free duplications.
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We manipulated progeny production by mating hermaphrodites to males, thereby increasing the availability of sperm and the level of progeny production.
These data suggest that substantially increasing the level of progeny production late in the reproductive period does not substantially alter somatic aging in WT hermaphrodites.
This is similar to the reported TLS efficiency of dG- N-AAF and dG-C8-AAF adducts transfected in COS-7 cells, but for knockdown of each of the pols, there was a reduction in the level of progeny from the C8-dG-ABA plasmid.
High levels of cross progeny production were positively correlated with extended longevity, and this relationship applied to total progeny production, cumulative progeny production through day 4, and progeny production on days 2, 4, and 5.
Here, using a longitudinal study, we observed that high levels of early progeny production were positively correlated with high levels of late progeny production.
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