In the fly, delayed reproduction also delays aging

Natural selection can modify the rate of aging. Often, the evolution of profoundly delayed (or negligible) senescence can be explained by thinking in reproductive terms: Organisms want to maximize production of descendants who are themselves well-situated to maximize their own reproductive success. Hence whales live long enough to help out their grandchildren, and the long lifespans of certain sessile species probably evolved because young organisms have to wait for older individuals to die before they can settle down to grow large and multiply (a similar phenomenon is likely operating on eusocial colonies).

In those examples, long life facilitates reproductive success. But what about the converse? Do species that evolve mechanisms to delay reproduction (e.g. under suboptimal conditions) achieve this goal by delaying aging, or do they let their biological clocks run on unhindered during reproductive arrest? At least in Drosophila, it appears that reproductive delay is also accompanied by a delay in the aging process. From Tatar et al.:

Negligible Senescence during Reproductive Dormancy in Drosophila melanogaster

Some endemic Drosophila overwinter in a state of adult reproductive diapause where egg maturation is arrested in previtellogenic stages. When maintained at cool temperatures, adult Drosophila melanogaster enter reproductive dormancy, that is, diapause or diapause-like quiescence. The ability to survive for extended periods is a typical feature of diapause syndromes. In adults this somatic persistence may involve reduced or slowed senescence. Here we assess whether reproductively dormant D. melanogaster age at slow rates. Adults were exposed to dormancy-inducing conditions for 3, 6, or 9 wk. After this period, demographic parameters were measured under normal conditions and compared to the demography of newly eclosed cohorts. The age-specific mortality rates of postdormancy adults were essentially identical to the mortality rates of newly eclosed, young flies. Postdormancy reproduction, in contrast, declined with the duration of the treatment; somatic survival during dormancy may tradeoff with later reproduction. Adults in reproductive dormancy were highly resistant to heat and to oxidative stress. Suppressed synthesis of juvenile hormone is known to regulate reproductive diapause of many insects. Treatment of dormant D. melanogaster with a juvenile hormone analog restored vitellogenesis, suppressed stress resistance, and increased demographic senescence. We conclude that D. melanogaster age at slow rates as part of their reproductive dormancy syndrome; the data do not agree with an alternative hypothesis based on heat-dependent “rate of living.” We suggest that low temperature reduces neuroendocrine function, which in turn slows senescence as a function of altered stress response, nutrient reallocation, and metabolism.

Postdormancy flies have the same mortality curve as young flies that never underwent the reproductive arrest — thus, they’ve delayed aging (in the sense of “the increased risk of dying per unit time as a function of chronological age”).

But not every aspect of the flies’ physiology is equally well preserved: Even though they’re surviving at the same rate, postdormancy flies are less fertile than young flies that have not experienced diapause — perhaps the endocrine systems that help preserve the somatic tissues are less efficient at maintaining the germ line. (The aging is of the fly germ line has been well studied in its own right, and is understood at sufficient molecular detail to allow very directed questions about how diapause affects the gonadal stem cell niche.)

That might seem to contradict the principle outlined above — that the purpose of delayed aging would be to increase reproductive success. If an organism’s fertility declines, who cares — in an evolutionary sense — how long it ultimately lives? The answer, I think, is to make the right comparison: The appropriate “control” for a postdormancy fly isn’t a young, well-fed compatriot that never encountered enviornmental conditions adverse enough to initiate diapause; rather, it’s the fly that died because it was dumping resources into reproduction when it should have been bolstering its stress responses and lining its body with fat in order to ride out the bad times. That fly’s fertility, obviously, is zero.



  1. Is this a surprising result? Was it not shown already that reduced fertility results in reduced aging?

    See: Carla M. Sgrò and Linda Partridge (1999). A Delayed Wave of Death from Reproduction in Drosophila. Science 286 (5449), 2521. [DOI: 10.1126/science.286.5449.2521]

  2. Thanks for the comment, Yoni.

    The Sgrò and Partridge study dealt with the increase in mortality resulting from early reproduction. This study deals with a decrease in mortality rates following a delay in reproduction.

    I suppose that whether or not you find it surprising depends on whether or not you feel like the truth of a proposition implies the truth of the converse proposition, which in biology it often doesn’t. That is to say, the earlier observation that reproduction increases mortality does not address the question of whether delaying reproduction decreases mortality.

  3. And yet delaying reproduction DOES extend lifespan–many studies have demonstrated that artificial selection on (early/late) reproduction produces (short/long) lifespans. (See classic papers by Luckinbill or Rose in the 1980s.)

    I think your point isn’t especially surprising because it is well demonstrated that the loci and/or mechanisms that affect longevity and reproduction are highly pleiotropic.

    Moreover, I think it’s important to point out that it’s rarely hypothesized that selection acts directly on longevity phenotypes. Rather, lifespan phenotypes evolve by indirect selection on something else–in melanogaster we have good evidence that these something elses are fecundity and the ability to enter reproductive diapause, depending upon environment.

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