Olsson Lab

Research Focus

Senescence

To what degree does ageing select for evolutionary change in phenotypic traits expressed during reproductive life? To what degree are the theories on the evolution of sexual reproduction and the evolution of senescence interconnected? We are testing the idea that in order for evolution to direct the senescence trajectory through an organism’s life, there needs to be heritable variation for the gerontological process, and this may be set already at fertilization, for example through genetic mate choice.

During aging, macromolecules accumulate damage, such as peroxidation of the lipids and erosion of the DNA, which results in malfunction of organelles. One hypothesis for explaining the overall effect of senescence is telomere loss. Teleomeres are the ‘caps’ on the ends of chromosomes that protect the chromosomes from erosion. In many species, teleomere length is inversely correlated with age and, thereby, can be used as an independent measure of ‘phenotypic ageing’. We are using staged experiments in the laboratory and monitoring of natural populations to investigate the following:

 

• Covariation between telomere shortening, testosterone and corticosterone levels and immunocapacity.
• Covariation between telomere length and probability of survival.
• Sexual dimorphism in telomere length an age-related immunocapcity.
• Telomere shortening in response to carotenoid treatment.