Evolutionary ecology of telomeres: a review

Abstract

Telomere-induced selection could take place if telomere-associated disease risk shortens reproductive life span and differently reduces relative fitness among individuals. Some of these diseases first appear before reproductive senescence and could thus influence ongoing selection. We ask whether we can estimate the components of the breeder's equation for telomeres, in which the response to selection (R, by definition "evolution") is the product of ongoing selection (S) and heritability (h 2 ). However, telomere inheritance is a conundrum: in quantitative genetics, traits can usually be allocated to categories with relatively high or low heritability, depending on their association with relative fitness. Telomere traits, however, show wide variation in heritability from zero to one, across taxa, gender, ethnicity, age, and disease status. In spite of this, there is divergence in telomere length among populations, supporting past and ongoing telomere evolution. Rates of telomere attrition and elongation vary among taxa with some, but not complete, taxonomic coherence. For example, telomerase is commonly referred to as "restricted to the germ line in mammals," but inbred mice and beavers have telomerase upregulation in somatic tissue, as do many ectotherms. These observations provoke a simplistic understanding of telomere evolutionary biology-clearly much is yet to be discovered.

FOXO1 and ETV6 genes may represent novel regulators of splicing factor expression in cellular senescence

“…This suggests that there may be some degree of disconnection between telomere erosion and senescence. Similarly, inbred strains of mice have somatic up-regulation of telomerase and comparatively long telomeres (47), yet still age. In our treated cells at least, the cell cycle blockade may be ameliorated by other signals, which remain to be elucidated.…”

Morph‐specific metabolic rate and the timing of reproductive senescence in a color polymorphic dragon

“…Indeed, the reduced metabolic rate we describe here is consistent with senescence manifest in weight loss, DNA damage, telomere shortening, and color fading across the breeding season in this species (Giraudeau et al., , Olsson, Tobler, Healey, Perrin, & Wilson, , Rollings et al., ). Telomere shortening and DNA damage is a hallmark of aging (Olsson, Wapstra, & Friesen, ). Telomeres are repetitive non‐coding DNA sequences and associated protective proteins located at the ends of eukaryote chromosomes.…”

“…Telomeres are repetitive non‐coding DNA sequences and associated protective proteins located at the ends of eukaryote chromosomes. Although their function is not fully understood, telomeres serve an important role in protecting the coding DNA from damage during cell division (Olsson et al., , Rollings, Miller, & Olsson, , Shalev, ). Higher metabolic rates are associated with more rapid cell division as well as higher production of reactive molecules that damage telomeres.…”

Long‐term effects of superoxide and DNA repair on lizard telomeres

“…At a cellular level, it is well accepted that oxidation compromises telomere length and attrition through a variety of mechanisms (Fouquerel, Parikh, & Opresko, ; von Zglinicki, ), a damage that is repaired in vivo but with varying success for a number of reasons. For example, contributing factors to this net attrition effect may be age‐ and sex‐specific dynamics in the production of telomerase, endogenous antioxidants (e.g., superoxide dismutase, catalase), and how the costs for the production of these enzymes are traded off against other self‐maintenance processes (Monaghan, ; Monaghan & Haussmann, ; Olsson, Wapstra, & Friesen, , ). In practice, any process that elevates metabolic rate and increases the level of not‐fully reduced oxygen, or fails to counter these effects with endo‐ or exogenous antioxidants, is a potential inducer of oxidative stress.…”

“…For example, increased testosterone levels (or reduced levels of oestrogen) may increase telomere attrition and explain sex differences in longevity (males often have shorter lives, Barrett & Richardson, ; Brooks & Garratt, ), with telomere shortening triggering cellular senescence (Valko et al., ). Given the benefits and costs (sometimes substantial) of “long” telomeres (increased risk of cancer; Olsson et al., , ), we therefore expect classic life history trade‐offs to be mediated by, or reflected in, telomere dynamics that should vary across taxa or morphs with different reproductive tactics.…”