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Density dependence triggers runaway selection of reduced senescence.

Seymour RM, Doncaster CP - PLoS Comput. Biol. (2007)

Bottom Line: Across a realistic spectrum of senescent age profiles, density regulation of recruitment can trigger runaway selection for ever-reducing senescence.The evolution of nonsenescence from senescence is robust to the presence of exogenous adult mortality, which tends instead to increase the age-independent component of vitality loss.We simulate examples of runaway selection leading to negligible senescence and even intrinsic immortality.

View Article: PubMed Central - PubMed

Affiliation: Department of Mathematics, University College London, London, United Kingdom.

ABSTRACT
In the presence of exogenous mortality risks, future reproduction by an individual is worth less than present reproduction to its fitness. Senescent aging thus results inevitably from transferring net fertility into younger ages. Some long-lived organisms appear to defy theory, however, presenting negligible senescence (e.g., hydra) and extended lifespans (e.g., Bristlecone Pine). Here, we investigate the possibility that the onset of vitality loss can be delayed indefinitely, even accepting the abundant evidence that reproduction is intrinsically costly to survival. For an environment with constant hazard, we establish that natural selection itself contributes to increasing density-dependent recruitment losses. We then develop a generalized model of accelerating vitality loss for analyzing fitness optima as a tradeoff between compression and spread in the age profile of net fertility. Across a realistic spectrum of senescent age profiles, density regulation of recruitment can trigger runaway selection for ever-reducing senescence. This novel prediction applies without requirement for special life-history characteristics such as indeterminate somatic growth or increasing fecundity with age. The evolution of nonsenescence from senescence is robust to the presence of exogenous adult mortality, which tends instead to increase the age-independent component of vitality loss. We simulate examples of runaway selection leading to negligible senescence and even intrinsic immortality.

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Related in: MedlinePlus

Graphs of Declining Vitality with Age(A) Decline in relative vitality with adult age given by Equation 12. For large x (x = 1), half the new-adult vitality is lost by an early age t1, whereas for small x (x = 0.1), it takes until age t2 to lose half the new-adult vitality. The curve x = 0 shows no senescence.(B) Decline in total vitality showing delayed-onset senescence, and also the tradeoff between senescence and new-adult fecundity, represented by the new-adult recruitment rate b0(x). The curve x = 0 shows no senescence. Here, the senescence rate is age dependent: 							, with n = 5, and b0(x) = 1 + x (further detailed in Appendix A of Text S1). In both panels, the nonsenescent mortality rate is μ0 = 0.01.
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pcbi-0030256-g001: Graphs of Declining Vitality with Age(A) Decline in relative vitality with adult age given by Equation 12. For large x (x = 1), half the new-adult vitality is lost by an early age t1, whereas for small x (x = 0.1), it takes until age t2 to lose half the new-adult vitality. The curve x = 0 shows no senescence.(B) Decline in total vitality showing delayed-onset senescence, and also the tradeoff between senescence and new-adult fecundity, represented by the new-adult recruitment rate b0(x). The curve x = 0 shows no senescence. Here, the senescence rate is age dependent: , with n = 5, and b0(x) = 1 + x (further detailed in Appendix A of Text S1). In both panels, the nonsenescent mortality rate is μ0 = 0.01.

Mentions: With this form, a large x determines early onset of significant decline in relative vitality shortly after adulthood, whereas a small x delays significant vitality loss to later ages (see Figure 1A). Delayed-onset vitality loss—i.e., the maintenance of a high level of relative vitality for a significant proportion of life history—can also be represented by age-dependent forms of the senescence rate, as discussed in Appendix A of Text S1. An example is illustrated in Figure 1B.


Density dependence triggers runaway selection of reduced senescence.

Seymour RM, Doncaster CP - PLoS Comput. Biol. (2007)

Graphs of Declining Vitality with Age(A) Decline in relative vitality with adult age given by Equation 12. For large x (x = 1), half the new-adult vitality is lost by an early age t1, whereas for small x (x = 0.1), it takes until age t2 to lose half the new-adult vitality. The curve x = 0 shows no senescence.(B) Decline in total vitality showing delayed-onset senescence, and also the tradeoff between senescence and new-adult fecundity, represented by the new-adult recruitment rate b0(x). The curve x = 0 shows no senescence. Here, the senescence rate is age dependent: 							, with n = 5, and b0(x) = 1 + x (further detailed in Appendix A of Text S1). In both panels, the nonsenescent mortality rate is μ0 = 0.01.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2230684&req=5

pcbi-0030256-g001: Graphs of Declining Vitality with Age(A) Decline in relative vitality with adult age given by Equation 12. For large x (x = 1), half the new-adult vitality is lost by an early age t1, whereas for small x (x = 0.1), it takes until age t2 to lose half the new-adult vitality. The curve x = 0 shows no senescence.(B) Decline in total vitality showing delayed-onset senescence, and also the tradeoff between senescence and new-adult fecundity, represented by the new-adult recruitment rate b0(x). The curve x = 0 shows no senescence. Here, the senescence rate is age dependent: , with n = 5, and b0(x) = 1 + x (further detailed in Appendix A of Text S1). In both panels, the nonsenescent mortality rate is μ0 = 0.01.
Mentions: With this form, a large x determines early onset of significant decline in relative vitality shortly after adulthood, whereas a small x delays significant vitality loss to later ages (see Figure 1A). Delayed-onset vitality loss—i.e., the maintenance of a high level of relative vitality for a significant proportion of life history—can also be represented by age-dependent forms of the senescence rate, as discussed in Appendix A of Text S1. An example is illustrated in Figure 1B.

Bottom Line: Across a realistic spectrum of senescent age profiles, density regulation of recruitment can trigger runaway selection for ever-reducing senescence.The evolution of nonsenescence from senescence is robust to the presence of exogenous adult mortality, which tends instead to increase the age-independent component of vitality loss.We simulate examples of runaway selection leading to negligible senescence and even intrinsic immortality.

View Article: PubMed Central - PubMed

Affiliation: Department of Mathematics, University College London, London, United Kingdom.

ABSTRACT
In the presence of exogenous mortality risks, future reproduction by an individual is worth less than present reproduction to its fitness. Senescent aging thus results inevitably from transferring net fertility into younger ages. Some long-lived organisms appear to defy theory, however, presenting negligible senescence (e.g., hydra) and extended lifespans (e.g., Bristlecone Pine). Here, we investigate the possibility that the onset of vitality loss can be delayed indefinitely, even accepting the abundant evidence that reproduction is intrinsically costly to survival. For an environment with constant hazard, we establish that natural selection itself contributes to increasing density-dependent recruitment losses. We then develop a generalized model of accelerating vitality loss for analyzing fitness optima as a tradeoff between compression and spread in the age profile of net fertility. Across a realistic spectrum of senescent age profiles, density regulation of recruitment can trigger runaway selection for ever-reducing senescence. This novel prediction applies without requirement for special life-history characteristics such as indeterminate somatic growth or increasing fecundity with age. The evolution of nonsenescence from senescence is robust to the presence of exogenous adult mortality, which tends instead to increase the age-independent component of vitality loss. We simulate examples of runaway selection leading to negligible senescence and even intrinsic immortality.

Show MeSH
Related in: MedlinePlus