Abstract
Telomeres are nucleoprotein structures that cap the end of each chromosome arm and function to maintain genome stability. The length of telomeres is known to shorten with each cell division and it is well-established that telomere attrition is related to replicative capacity in vitro. Moreover, telomere loss is also correlated with the process of aging in vivo. In this review, we discuss the mechanisms that lead to telomere shortening and summarise telomere homeostasis in humans throughout a lifetime. In addition, we discuss the available evidence that shows that telomere shortening is related to human aging and the onset of age-related disease.
Highlights
Structure, Function and Maintenance of the TelomereTelomeres are nucleoprotein structures found at the end of each chromosome arm that function to maintain genome stability
It is important that telomere length is maintained to ensure prolonged replicative capacity and this is achieved via two primary mechanisms: The action of a specialised enzyme called telomerase or homologous recombination mediated alternative lengthening of telomeres (ALT)
Since their discovery in 1939, our knowledge of telomere biology has continued to advance in leaps and bounds
Summary
Telomeres are nucleoprotein structures found at the end of each chromosome arm that function to maintain genome stability. Telomeres are formed of a highly conserved, hexameric (TTAGGG) tandem repeat DNA sequence This is organised into a looped structure called a T-loop and associated with specialised proteins including, among others, those that make up the Shelterin complex [1,2,3]. The looped structure (Figure 1) is formed via nucleolytic activity at the extreme termini of telomeric DNA to produce a single stranded G-rich overhang. The presence and action of these proteins at the telomere sequence is largely governed by proteins that make up the Shelterin complex This complex is made up of a collection of six specialized proteins that associate with the telomere structure to form a fully functional capping structure.
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