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Senescence is a common process to almost all multicellular organisms4, although it is true that some types of organisms such as certain coelenterates not experience any decline in fitness with age12. Furthermore, senescence is not observed either in unicellular organisms such as prokaryotes12. We could define senescence as those time-dependent changes occurring in the body and adversely affect its functions, resulting in a constant decline in biological fitness due to the internal physiological deterioration8, 12. In natural populations this would be manifested as an increase in the probability of death and a decrease in reproductive success10.
Although many manuscripts often use the term aging, I use preferably senescence instead of aging because the latter would be mainly associated with any phenotypic age-related change without emphasize the adverse effects that the term senescence implies9.
Many biologists conceive the senescence as an inevitable process of damage accumulation, as happens with objects or cars, which leads to the loss of certain functions and finally to the death9, 3. However, the existence of high variability in the rate of aging among multicellular organisms reveals that senescence is a process subject to change and therefore to selection3, 10.
The classic evolutionary theory of senescence try to give a satisfactory explanation to this seemingly paradoxical process, since a decline in the individuals fitness with age should be counteracted by selection5. The two major contributors to this theory were Medawar and Williams, who proposed two mechanisms of action for this process, and Hamilton, who later formalized the theory6.
Basically, the evolutionary theory of senescence postulates that as age increases, the strength of selection on the deleterious or partially deleterious alleles decreases because only few individuals carrying such alleles are still alive to express them11. This reduced survival is due to the increasing probability of succumbing to some extrinsic factor with age, such as predation or disease9, 15. In addition, older individuals also experience a decline in fertility, contributing less to the gene pool of future generations9. However, this generalization does not apply to species that grow and increase their fertility throughout their life as do some fish and turtles9.
As mentioned above, Medawar and Williams postulated two modes of action in which selection could operate to shape the patterns of senescence. Medawar in 1952 suggested that deleterious mutations would accumulate as the individual's life passes, and this accumulation would reduce the survival of their bearers (mutation accumulation theory)9. This approach is rather simplistic for many evolutionary biologists because it implies that the strength of selection is only too weak in older ages. Moreover, this decline could be explained without the need of senescence, only referring to factors of extrinsic mortality which would provide enough evidence for the decline in the force of natural selection9.
Another weakness of this theory is the prediction about the sharp increase in mortality rates after the age at which the strength of selection is 0, usually after the last breeding season. The data show that does not exist a sudden increase in mortality rate due to the greater accumulation of deleterious mutations with age, and even more, the mortality rate remains constant (mortality plateaus) or is lower10. However, this was partially solved in age-structured populations by Charlesworth, who propose the modified mutation accumulation model. In such model mortality plateaus can be predicted if deleterious alleles affect more than one age class or reduced fitness accumulates in all classes after a given age7.
Later, in 1957, Williams postulate his antagonistic pleiotropy theory. His approach is based on the existence of genes with pleiotropic effects that would have positive effects, favouring survival and reproduction, during early stages in the life of an organism but would have deleterious effects at older ages. These genes would be strongly selected in early stages of life by improving fitness although their late-life effects lead to a decrease of it. The bearers of these genes would be maintained in the population at older ages due to a decline in the force of selection at these ages9, 7.
Following this theory, the disposable soma would arise proposed by Kirkwood in 19779. He exposes here the trade-off to distribute resources between vital functions such as damage repair and reproduction. Once the resources are concentrated mainly in reproduction, the metabolic damage begins to increase due to lack of supply in the repair and maintenance, being accumulated over the time9. Therefore, the disposable soma theory could be defined as the phenotypic version of the antagonistic pleiotropy since an allele that increases energy allocation to reproduction has the opposite effect of reducing the resources for maintenance and repair4.
The main difference between these two evolutionary mechanisms for senescence would be that the mutation accumulation process is passive, meaning that only mutation would intervene as a force of evolutionary change, whereas in antagonistic pleiotropy selection would be primarily responsible for maintenance of such alleles in the gene pool7. Therefore, knowing that usually the mutation rate is very low in most multicellular organisms we can say that, even if possible, its importance is not enough to explain the evolution of senescence10. However, we must stress that the two mechanisms are not mutually exclusive and both may operate concurrently7.
On the other hand, recently some researchers have proposed new evolutionary theories of senescence in an attempt to associate it to other processes that affect life histories. From this effort emerged the social theory of aging, based on kin selection, which suggests that sociality influences the pattern of aging since mortality and longevity at the individual level could affect the fitness of other related individuals. This is particularly true for those species that take care of their offspring after birth9. In these species, with a trade-off in the number of offspring due to the costs of postreproductive care, only the effect of intergenerational transfers accounts for their mortality patterns and prolonged survival after reproduction6.
Thus, the classical theories would not be enough to explain the evolution of senescence in those species which make investments in the offspring after birth because these investments are important for their survival, growth and reproductive success, having to appeal to other explanations such as the intergenerational transfer effect which sort out the evolution towards lower fertility, longer postreproductive survival and the trade-off optimization between quantity-quality6.
One of the most far-reaching predictions of the classical theory is that species or individuals with lower extrinsic mortality rates should evolve towards lower rates of aging and therefore to an increase in lifespan4, 5, 2. In insects, which are characterized by high extrinsic mortality and rapid senescence, however, we can find strong support for this prediction. The defense of this prediction finds a solid basis in eusocial insects like ants, termites and bees, but we will focus mainly on the world of ants4.
First, the evidence comes from the extreme longevity in ant queens4, 5. Since the queens in most social insects are highly protected from any external risk and are virtually immune to predation once they have established a colony, they should experience a longer lifespan than solitary insects, and so illustrate the results of Keller & Genoud (1997).
Fig. 1. Mean lifespans for solitary insects and queens from highly eusocial insects. As we can see, the avoidance of extrinsic mortality allows queens of eusocial insects to develop incredible long lifespans, reaching in some cases 28 years old. (Figure taken from Keller & Gonaud 1997).
In addition, there are significant differences in life expectancy according to the strategy adopted: monogyny (single queen in the colony) or polygyny (multiple queens in the colony). Note that ant species with multiple queens are subject to greater extrinsic risk because of their lack of complex nests and frequent changes in location, while monogyny species often develop a heavily guarded complex structure for queens. This is also usually related with the time that they produce their first fertile generation, being generally later in monogyny species5.
The second set of evidence comes from the differentiation of tasks in the ant Oecophylla smaragdina. In this species worker castes are divided into two groups: large workers who perform tasks of resource provisioning and defense, and small workers who care for the offspring in the nest. According to evolutionary theory, larger workers will age earlier because they are more exposed to external risks, and this is what Chapuisat & Keller (2002) have observed, providing arguments against purely mechanistic theories of senescence which presuppose a longer lifespan associated with increased body size2.
Fig. 2. Large worker of the weaver ant Oecophylla smaragdina.
(Picture taken from www.bukisa.com)
Furthermore, the comparison between individuals of different castes with identical genomes which are expressed differently due to environmental factors allows us to understand the relative contribution of both mechanisms to the evolution of senescence. The late-life mutation accumulation could only occur in castes that have shorter lifespans because in castes with longer lifespans these mutations would be inactivated allowing longer lifespan. Moreover, senescence could be explained as a compromise between somatic maintenance and other functions that would increase the individual or colony fitness, that is, the differentially expressed genes in each caste will have been selected if the productivity of the colony increases2.
These two sets of evidence support the classical evolutionary theory illustrating the predictions that it raises. In addition, they also show the limited contribution of the mutation accumulation in relation with antagonistic pleiotropy theory, as pointed out by other authors10. Moreover, the integration of senescence with other vital processes is essential to get better understanding of this process and the future research should be addressed in that way. Finally, organisms such as eusocial insects could be a good alternative to the classical model organisms for the study of senescence evolution since their worker castes are genetically identical and they do not reproduce, opening a new stimulating spectrum of possibilities to elucidate the mechanisms involved in senescence2.