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All's well that ends well? Causes of variation in telomere length

Subject Area Animal Physiology and Biochemistry
Sensory and Behavioural Biology
Evolution, Anthropology
Evolutionary Cell and Developmental Biology (Zoology)
Term from 2015 to 2017
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 278198414
 
Final Report Year 2017

Final Report Abstract

Telomeres are evolutionarily conserved DNA sequence repeats, which together with proteins form the ends of chromosomes and function in genome stability. Telomere length is increasingly used as a biomarker of ageing and health, as telomeres shorten with age and “life stress”, and short telomeres, independent of age, have been shown to relate to reduced survival probability in many organisms including humans and birds. Between individuals of the same age telomeres differ significantly in length and the goal of this project was to unravel how this variation in telomere lengths arises, more specifically, to investigate (i) inheritance of telomere length and (ii) physiological mechanisms related to telomere attrition. To address these questions, the project uses a long-term, individual based study population of free-living jackdaws Corvus monedula, where birds are of known age, sex and relatedness. Blood samples for telomere analysis were taken from nestlings as well as during adulthood since 2005. Telomere length has been measured using telomere restriction fragment analysis, which is currently considered the golden standard method for telomere length determination in the fields of epidemiology, evolution and ecology. Based on a pedigree spanning 5 generations, including more than 1000 jackdaws that contributed relatedness information and more than 700 individuals with known telomere length, heritability has been estimated to explain 68% of the variation of telomere length soon after hatching. This high heritability value supports the finding of the largest study on humans, while results of other studies range from no heritability of telomere length to almost 100%. Additionally, we identified paternal age to contribute to telomere length variation. We showed that as fathers become older they produced offspring with shorter telomeres, while mother age had no effect. This result did not differ for offspring, which was raised by foster parents. Thus, it was an effect of the age of the genetic father and not an age effect based on parental care. Further, telomere attrition of the genetic father with age, measured in the blood, predicted the telomere length of the offspring he produced over years. These results support an epigenetic inheritance mechanism. Life stress and environmental conditions have been shown to influence telomere attrition. It has been suggested that the process of telomere attrition may be modulated by the physiological stress response and involve the “stress” hormone corticosterone. We first tested this prediction in a dataset on common terns Sterna hirundo, where individuals with high reproductive success had shorter telomeres. We showed that in males, which do most of the chick provisioning in this species, high corticosterone concentrations were associated with high reproductive success and short telomeres. Further, we related corticosterone levels to telomere attrition in jackdaw nestlings. Nestlings with higher corticosterone levels measured in the feathers grown during the nestling phase experienced a higher telomere attrition in the same time period. Findings of both studies suggest a relationship between corticosterone concentration and telomere attrition. As corticosterone is mainly a signalling hormone, it remains to investigate how those mechanisms are linked. Studies in cell cultures have shown that oxidative stress shortens telomeres. If oxidative stress in naturally occurring concentrations in an organism leads to telomere shortening is not well known. Therefore, we measured six different parameters of oxidative stress in jackdaw nestlings and related it to their telomere attrition during the nestling phase. We did not find any correlation between oxidative stress and telomere attrition. A potential explanation is that cell division, which is known to shorten telomeres due to incomplete DNA replication, is the main reason for telomere attrition and potential shortening due to oxidative stress is comparatively low.

Publications

  • (2016) Telomere length reflects reproductive effort indicated by corticosterone levels in a long-lived seabird. Molecular Ecology, 25: 5785-5794
    Bauch C, Riechert J, Verhulst S, Becker PH
    (See online at https://doi.org/10.1111/mec.13874)
  • (2017) Does oxidative stress shorten telomeres? Biology Letters, 13: 20170164
    Boonekamp JJ, Bauch C, Mulder E, Verhulst
    (See online at https://doi.org/10.1098/rsbl.2017.0164)
 
 

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