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The mechanisms that underlie senescence are not well understood in insects. Telomeres are conserved repetitive sequences at chromosome ends that protect DNA during replication. In many vertebrates, telomeres shorten during cell division and in response to stress and are often used as a cellular marker of senescence. However, little is known about telomere dynamics across the lifespan in invertebrates. We measured telomere length in larvae, prepupae, pupae, and adults of two species of solitary bees,Osmia lignariaandMegachile rotundata. Contrary to our predictions, telomere length was longer in later developmental stages in bothO. lignariaandM. rotundata.Longer telomeres occurred after emergence from diapause, which is a physiological state with increased tolerance to stress. InO. lignaria, telomeres were longer in adults when they emerged following diapause. InM. rotundata, telomeres were longer in the pupal stage and subsequent adult stage, which occurs after prepupal diapause. In both species, telomere length did not change during the 8 months of diapause. Telomere length did not differ by mass similarly across species or sex. We also did not see a difference in telomere length after adultO. lignariawere exposed to a nutritional stress, nor did length change during their adult lifespan. Taken together, these results suggest that telomere dynamics in solitary bees differ from what is commonly reported in vertebrates and suggest that insect diapause may influence telomere dynamics.

 

Abstract Although the pace of senescence varies considerably, the physiological systems that contribute to different patterns of senescence are not well understood, especially in long-lived vertebrates. Long-lived bony fish (i.e., Class Osteichthyes) are a particularly useful model for studies of senescence because they can readily be aged and exhibit some of the longest lifespans among vertebrates. In this study we examined the potential relationship between age and multiple physiological systems including: stress levels, immune function, and telomere length in individuals ranging in age from 2 to 99 years old in bigmouth buffalo ( Ictiobus cyprinellus ), the oldest known freshwater teleost fish. Contrary to expectation, we did not find any evidence for age-related declines in these physiological systems. Instead, older fish appeared to be less stressed and had greater immunity than younger fish, suggesting age-related improvements rather than declines in these systems. There was no significant effect of age on telomeres, but individuals that may be more stressed had shorter telomeres. Taken together, these findings suggest that bigmouth buffalo exhibit negligible senescence in multiple physiological systems despite living for nearly a century. 

Telomeres, protective caps at the end of chromosomes, are often positively related to lifespan and are thought to be an important mechanism of organismal aging. To better understand the casual relationships between telomere length and longevity, it is essential to be able to experimentally manipulate telomere dynamics (length and loss rate). Previous studies suggest that exposure to TA‐65, an extract from the Chinese rootAstragalus membranaceus, activates telomerase, lengthens telomeres, increases the growth of keratin‐based structures, and boosts the immune system in adults. However, telomere loss is expected to be greatest during early life but whether TA‐65 has similar effects during this life stage is currently unknown. Here, we experimentally exposed free‐living house sparrow (Passer domesticus) chicks to TA‐65 during post‐natal development and examined the effects on telomere length and loss, growth of keratin‐based structures, and a measure of cellular immunity. Contrary to expectation, the growth of keratin‐based structures was reduced in TA‐65 chicks and in the second year of the study, chicks exposed to TA‐65 experienced more telomere loss than controls. Thus, the effects of TA‐65 on telomeres and keratin‐based structures differ across life stages and future research will be necessary to determine the mechanisms underlying these age‐specific effects.