Senescence as an adaptation to limit the spread of disease

Mitteldorf, Josh; Pepper, John W.

doi:10.1016/j.jtbi.2009.05.013

Cited by 65 publications

(42 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Life-history theory posits that key events during an organism's life, such as the rate of juvenile development, age of first reproduction, number of offspring produced and the rate of senescence (Mitteldorf and Pepper, 2009;Longo et al, 2005), are shaped by natural selection to produce the largest possible number of surviving offspring (Stearns, 1992). Variation in life-history events is thought to reflect the differential allocation of resources, time and/or energy to competing life functions, largely growth, body maintenance and reproduction (Charnov, 1993;Ghalambor and Martin, 2001).…”

Section: Introductionmentioning

confidence: 99%

Linkages between the life-history evolution of tropical and temperate birds and the resistance of their cells to oxidative and non-oxidative chemical injury

Jiménez

Harper

Queenborough

et al. 2012

Journal of Experimental Biology

View full text Add to dashboard Cite

SUMMARYA fundamental challenge facing physiological ecologists is to understand how variation in life history at the whole-organism level might be linked to cellular function. Thus, because tropical birds have higher annual survival and lower rates of metabolism, we hypothesized that cells from tropical species would have greater cellular resistance to chemical injury than cells from temperate species. We cultured dermal fibroblasts from 26 tropical and 26 temperate species of birds and examined cellular resistance to cadmium, H 2 O 2 , paraquat, thapsigargin, tunicamycium, methane methylsulfonate (MMS) and UV light. Using ANCOVA, we found that the values for the dose that killed 50% of cells (LD 50 ) from tropical birds were significantly higher for H 2 O 2 and MMS. When we tested for significance using a generalized least squares approach accounting for phylogenetic relationships among species to model LD 50 , we found that cells from tropical birds had greater tolerance for Cd, H 2 O 2 , paraquat, tunicamycin and MMS than cells from temperate birds. In contrast, tropical birds showed either lower or no difference in tolerance to thapsigargin and UV light in comparison with temperate birds. These findings are consistent with the idea that natural selection has uniquely fashioned cells of long-lived tropical bird species to be more resistant to forms of oxidative and non-oxidative stress than cells from shorterlived temperate species.Supplementary material available online at

show abstract

Section: Introductionmentioning

confidence: 99%

Linkages between the life-history evolution of tropical and temperate birds and the resistance of their cells to oxidative and non-oxidative chemical injury

Jiménez

Harper

Queenborough

et al. 2012

Journal of Experimental Biology

View full text Add to dashboard Cite

show abstract

“…Elsewhere, (Mitteldorf and Pepper 2007) we have noted that the advantage of keeping infectious outbreaks in check is a well-recognized evolutionary force in the context of the evolution of sex (Bell 1982). This is an application of the Red Queen Hypothesis (van Valen 1973).…”

Section: Resultsmentioning

confidence: 99%

“…We suggest that these observations are consistent with a group-selective mechanism, in which infectious epidemics favor modest population densities. In an environment where infectious disease provides a powerful incentive for population densities to remain modest, it is possible for limits on life span to evolve as an adaptation (Mitteldorf and Pepper 2007).…”

Section: The Argument From Genotype By Environment Interactionmentioning

confidence: 99%

How can evolutionary theory accommodate recent empirical results on organismal senescence?

Mitteldorf

Pepper

2007

Theory Biosci.

View full text Add to dashboard Cite

According to a prominent recent report, guppies collected from sites lacking predators are inferior in every aspect of their life history profile to those evolved in other, nearby sites with predators present. This is an exception to two classical predictions of evolutionary theory: that low extrinsic mortality should be associated with longer life span, and that higher fertility should be associated with shorter life span. Some theorists have tried to accommodate this and other anomalous results within the standard framework, but we argue that the exceptions they carve out do not explain the results at hand. In fact, the findings suggest that population regulation has been selected at the group level, though this is a mechanism that most theorists regard with suspicion. We conclude by relating the present result to other experiments that seem to point in the same direction.

show abstract

“…Aging may evolve ''opportunistically'' for reasons that have nothing to do with population dynamics. Aging offers a selective advantage for population turnover (Martins 2011), contributes to evolvability (Mitteldorf and Martins 2014), and helps diversify the population to protect against infectious epidemics (Mitteldorf and Pepper 2009). …”

Section: Introductionmentioning

confidence: 99%

An epigenetic clock controls aging

Mitteldorf¹

2015

Biogerontology

Self Cite

View full text Add to dashboard Cite

We are accustomed to treating aging as a set of things that go wrong with the body. But for more than twenty years, there has been accumulating evidence that much of the process takes place under genetic control. We have seen that signaling chemistry can make dramatic differences in life span, and that single molecules can significantly affect longevity. We are frequently confronted with puzzling choices the body makes which benefit neither present health nor fertility nor long-term survival. If we permit ourselves a shift of reference frame and regard aging as a programmed biological function like growth and development, then these observations fall into place and make sense. This perspective suggests that aging proceeds under control of a master clock, or several redundant clocks. If this is so, we may learn to reset the clocks with biochemical interventions and make an old body behave like a young body, including repair of many of the modes of damage that we are accustomed to regard as independent symptoms of the senescent phenotype, and for which we have assumed that the body has no remedy.

show abstract

Senescence as an adaptation to limit the spread of disease

Cited by 65 publications

References 44 publications

Linkages between the life-history evolution of tropical and temperate birds and the resistance of their cells to oxidative and non-oxidative chemical injury

Linkages between the life-history evolution of tropical and temperate birds and the resistance of their cells to oxidative and non-oxidative chemical injury

How can evolutionary theory accommodate recent empirical results on organismal senescence?

An epigenetic clock controls aging

Contact Info

Product

Resources

About