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Evolutionary EcologyConcepts and Case Studies$
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Charles W. Fox, Derek A. Roff, and Daphne J. Fairbairn

Print publication date: 2001

Print ISBN-13: 9780195131543

Published to Oxford Scholarship Online: November 2020

DOI: 10.1093/oso/9780195131543.001.0001

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PRINTED FROM OXFORD SCHOLARSHIP ONLINE (oxford.universitypressscholarship.com). (c) Copyright Oxford University Press, 2021. All Rights Reserved. An individual user may print out a PDF of a single chapter of a monograph in OSO for personal use. date: 17 June 2021

Senescence

Senescence

Chapter:
(p.128) 10 Senescence
Source:
Evolutionary Ecology
Author(s):

Marc Tatar

Publisher:
Oxford University Press
DOI:10.1093/oso/9780195131543.003.0015

At all taxonomic levels, there exists tremendous variation in life expectancy. A field mouse Peromyscus may live 1.2 years, while the African elephant may persist for 60 years, and even a mousesized bat such as Corynorhinus rafinesquei lives a healthy 20 years (Promislow 1991). Part of this variance is caused by differences in ecological risks, rodents being perhaps the most susceptible to predation, and to vagaries of climate and resources. Another portion is caused by differences in senescence, the intrinsic degeneration of function that produces progressive decrement in age-specific survival and fecundity. Senescence occurs in natural populations, where it affects life expectancy and reproduction as can be seen, for instance, from the progressive change in age-specific mortality and maternity of lion and baboon in East Africa. The occurrence of senescence and of the widespread variation in longevity presents a paradox: How does the age-dependent deterioration of fitness components evolve under natural selection? The conceptual and empirical resolutions to this problem will be explored in this chapter. We shall see that the force of natural selection does not weigh equally on all ages and that there is therefore an increased chance for genes with late-age-deleterious effects to be expressed. Life histories are expected to be optimized to regulate intrinsic deterioration, and in this way, longevity evolves despite the maladaptive nature of senescence. From this framework, we will then consider how the model is tested, both through studies of laboratory evolution and of natural variation, and through the physiological and molecular dissection of constraints underlying trade-offs between reproduction and longevity. As humans are well aware from personal experience, performance and physical condition progressively deteriorate with adult age. And in us, as well as in many other species, mortality rates progressively increase with cohort age. Medawar (1955), followed by Williams (1957), stated the underlying assumption connecting these events: Senescent decline in function causes a progressive increase in mortality rate. Although mortality may increase episodically across some age classes, such as with increases in reproductive effort, we assume that the continuous increase of mortality across the range of adult ages represents our best estimate of senescence.

Keywords:   Antioxidant systems, Biogerontology, Cohort life tables, Demographic senescence, Free radicals, Gompertz, Heat shock proteins, Induced expression, Maximum likelihood methods

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