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Mutation and Senescence: Where Genetics and Demography Meet

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Mutation and Senescence: Where Genetics and Demography Meet Genetica 102/103: 299–314, 1998. 299 c 1998 Kluwer Academic Publishers. Printed in the Netherlands. Mutation and senescence: where genetics and demography meet Daniel E.L. Promislow1 & Marc Tatar2 1 Department of Genetics, University of Georgia, Athens, GA 30602-7223, USA (Phone: (706) 542-1715; Fax: (706) 542-3910; E-mail: [email protected]); 2 Department of Ecology and Evolutionary Biology, Brown University, Providence, RI 02912, USA (E-mail: mark [email protected]) Key words: mutation accumulation, senescence, demography, mortality Abstract Two evolutionary genetic models–mutation accumulation and antagonistic pleiotropy–have been proposed to explain the origin and maintenance of senescence. In this paper, we focus our attention on the mutation accu- mulation model. We re-examine previous evidence for mutation accumulation in light of new information from large-scale demographic experiments. After discussing evidence for the predictions that have been put forth from models of mutation accumulation, we discuss two critical issues at length. First, we discuss the possibility that classical fruit fly stock maintenance regimes may give rise to spurious results in selection studies of aging. Second, we consider evidence for the assumptions underlying evolutionary models of aging. These models assume that mutations act additively on age-specific survival rate, that there exist mutations whose effects are confined to late age-classes, and that all mutations have equal effects. Recent empirical evidence suggests that each of these three assumptions is unlikely to be true. On the basis of these results, we do not conclude that mutation accumulation is no longer a valid explanation for the evolution of aging. Rather, we suggest that we now need to begin developing more biologically realistic genetic models for the evolution of aging. Introduction oretical and empirical work in the field with recent advances in the use of large-scale demography in stud- Other authors, including many in this volume, have ies of senescence (Carey et al., 1992; Curtsinger et al., described how mutations can act not only as the source 1992; Vaupel, Johnson & Lithgow, 1994). In light of of genetic variation on which selection acts, but may these studies, we focus on the ways in which an explic- even be the fundamental driving force in evolutionary itly demographic perspective can enhance our ability to change, from the origin of sex (Kondrashov, 1998) to interpret studies of mutation accumulation and aging, the maintenance of sexually selected characters (Pomi- and guide research in the future. ankowski, Iwasa & Nee, 1991) to the ultimate decline and disappearance of populations (Lande, this vol- ume). Here we turn our attention to the evolution of Background aging. Many previous books and articles have provided Aging is here defined as a persistent decline in age- comprehensive reviews of the underlying theory for specific fitness components of an organism (i.e., rates the evolution of aging and the evidence that supports of reproduction and survival) due to internal physio- or refutes this theory (Rose & Charlesworth, 1980; Par- logical deterioration (Rose, 1991). We expect to see an tridge & Barton, 1993; Charlesworth, 1994; Curtsinger age-related decline in all fitness components. For the et al., 1995). Rather than revisit this body of work, we purpose of this present article we focus our attention will touch on the theoretical background only briefly. on age-specific mortality rates (Comfort, 1979; Finch, Our primary aim here is to integrate previous the- Pike & Witten, 1990; Promislow, 1991; Curtsinger, MENNEN/Preproof/Art: Pips Nr.:159825; Ordernr.:235573-mc; sp.code:A441WO BIO2KAP gene441.tex; 26/05/1998; 15:02; v.7; p.1 300 1995), while acknowledging that other metrics of aging mulation model of aging. Second, we explore the spe- exist (Curtsinger, 1995; Graves, 1995; Partridge & cific problem that arises in tests of aging due to the Barton, 1996). way in which fruit flies – the work-horse of the field of The evolutionary origins of senescence are gen- experimental demography – are maintained. And final- erally explained by two widely-accepted theories– ly, we weigh the evidence in support of the underlying mutation accumulation (Medawar, 1952) and antag- assumptions of evolutionary models of aging. onistic pleiotropy (Williams, 1957). We will confine our focus here to the mutation accumulation model. Medawar (1952) proposed that senescence arises Evidence for the mutation accumulation model because the strength of selection declines with age. A newly arising mutation in humans that reduces fertil- The mutation accumulation model gives rise to numer- ity by 50%, but that is only expressed after age 45, ous predictions that can be tested experimentally: a) would experience little selection against it. In the vir- variance for fitness traits should increase with age tual absence of selection, it may increase in frequen- (Rose & Charlesworth, 1981b; Charlesworth, 1990); cy through drift alone. The same deleterious muta- b) reverse selection for early fitness on lines produced tion expressed at age 20 would be subject to very from selection for late-life fitness should only slow- strong selection. As a consequence, over many gen- ly revert to pre-selection age-specific phenotypes; c) erations, late-acting deleterious mutations are more the controlled introduction of spontaneous or directed likely to accumulate than early-acting ones. These mutations should alter patterns of senescence; and d) late-acting mutations will then cause an age-related inbreeding depression should increase with age (Tana- decline in fitness traits, including fecundity, fertili- ka, 1993; Charlesworth & Hughes, 1996). ty, and survival rates. This theory of aging has given rise to specific micro-evolutionary predictions (Rose, A. Changes in variance with age 1985; Charlesworth, 1990). In particular, mathemati- cal models of Medawar’s mutation accumulation the- Under the mutation accumulation scenario, the rela- ory predict an age-related increase in genetic variance tively reduced force of natural selection permits an components (Charlesworth, 1990) and in inbreeding age-dependent decrease in the selection-mutation bal- load (Charlesworth & Hughes, 1996) for traits related ance. This should lead, in turn, to a greater amount of to fitness. additive genetic variance for fitness traits at late ages Charlesworth’s models (Charlesworth, 1990; compared to earlier ages. The prediction of an age- Charlesworth, 1994; Charlesworth & Hughes, 1996) related increase in genetic variance for fitness compo- are based on assumptions about the nature of the effects nents is fundamental(though not necessarily exclusive, of mutations on fitness components. To make analy- see Charlesworth & Hughes, 1996) to the mutation sis tractable, while acknowledging that the assump- accumulation theory of aging. Many studies have now tions underlying the model are not necessarily realistic, tested this prediction for a variety of traits, including Charlesworth has made the simplifying assumptions age-specific fecundity (Rose & Charlesworth, 1981b; that mutations act additively on age-specific survival Engstrom¨ et al., 1989; Ebert, Yampolsky & Van rates and that mutations are equally likely to act at any Noordwijk, 1993; Tanaka, 1993; Tatar et al., 1996), age. We address the experimental evidence for these age-specific mortality (Hughes & Charlesworth, 1994; assumptions in a later section of this paper. Hughes, 1995; Promislow et al., 1996), and male repro- Both mutation accumulation and antagonistic ductive ability (Kosuda, 1985; Hughes, 1995), with pleiotropy theories have spawned a wealth of mixed results. experimental tests (recent reviews in Rose, 1991; Charlesworth, 1994). But only very recently have biol- Fecundity ogists recognized that to understand the evolution of Rose and Charlesworth (1980, 1981b) first tested this aging fully, genetic studies of survival or fecundity prediction by analyzing additive genetic variation for need to rest on large-scale demographic approaches fecundity in Drosophila melanogaster. Average addi- (e.g., Curtsinger et al., 1992; Curtsinger et al., 1995; tive genetic variance did not change with age. How- Fukui, Ackert & Curtsinger, 1996). With this in mind, ever, as has been previously pointed out, any realized we first use a demographic perspective to evaluate increase in variance may have been offset by the dif- existing experimental evidence for the mutation accu- gene441.tex; 26/05/1998; 15:02; v.7; p.2 301 ferential mortality of females with relatively high ear- ance, subsequent work by Hughes (1995) demonstrates ly fecundity, due to the costs of reproduction (Clark, a similar increase in additive genetic variance for male 1987; Engstrom¨ et al., 1989; Partridge & Barton, mating ability. 1993). In a later study, Engstrom¨ et al. (1989) included B. Demographic selection only those females that survived for the duration of the experiment. Although they found that variance for Lines generated by demographic selection have been fecundity increased with age, the observed increase used to assess whether mutation accumulation caus- may have been due to the fact that their data were log- es senescence. Service, Hutchinson and Rose (1988) transformed (G. Engstrom,¨ personal communication; applied reverse selection to lines that had originally Tatar et al., 1996), when the underlying raw data were been selected for postponed senescence. After reverse not log-normally distributed. selection they
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