Abstract
Changes of telomere length with age were assessed in diploid and triploid rainbow trout (Oncorhynchus mykiss) females in the cross-sectional study using Q-FISH technique. Triploid trout as sterile do not invest an energy in gametogenesis and continue to grow, whereas fertile diploid individuals suffer from declines in growth and survival during sexual maturation. However, triploid and diploid specimens exhibited similar patterns of telomere dynamics. Telomere length in the embryos, larvae and one-year-old juveniles did not change significantly. In the second year after hatching, subadults exhibited substantially shortened telomeres, while significant increase of the telomere length was reported in the three-year-old adults. On the other hand, correlation between telomere length and body size was observed in the triploid, but not in the diploid rainbow trout. Telomere shortening observed in two-year-old subadults may have been associated with the premature period of the fast growth in rainbow trout. Similar pattern of the telomere dynamics reported in the fertile diploids and sterile triploids indicated processes related to reproduction did not affect telomere dynamics in this species. Unexpected increase of the telomere length reported during the third year of life confirmed that in rainbow trout telomeric DNA shortens and lengthens, depending on the developmental stage.
Highlights
Telomeres are nucleoprotein complexes at the ends of eukaryotic chromosomes
In this research we reported age-related decrease and increase of telomere length in the diploid and triploid rainbow trout
After substantial telomere loss observed in the two-year-old rainbow trout, telomere length in the three-year-old diploids and triploids was increased to reach the size observed in the one-year-old juveniles (Figure 1)
Summary
Telomeres are nucleoprotein complexes at the ends of eukaryotic chromosomes. In all vertebrates studied to date, the DNA component of the telomeres contains tandemly repeated G-rich hexanucleotide sequence (TTAGGG/CCCTAA)n [1]. Telomeres protect chromosomes from end-to-end fusions and degradation, guarantee their complete replication and allow DNA repair machinery to distinguish natural chromosomal ends from the ends that appear in the course of breakage events [2,3]. As the DNA polymerase is not able to replicate ends of linear chromosomes (“end replication problem”). Attrition of telomeres is accelerated by the oxidative stress associated with increased production of reactive oxygen species (ROS) [5]. Rich in guanine telomeric DNA is susceptible to damage from ROS and many experiments confirmed that oxidative stress increases incidences of the DNA strand breaks leading to loss of distal telomere fragments [7]. The process of telomere loss may be compensated mainly by the telomerase, an enzyme
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