Abstract
Telomeres comprise the ends of eukaryotic chromosomes and are essential for cell proliferation and genome maintenance. Telomeres are replicated by telomerase, a ribonucleoprotein (RNP) reverse transcriptase, and are maintained primarily by nucleoprotein complexes such as shelterin (TRF1, TRF2, TIN2, RAP1, POT1, TPP1) and CST (Cdc13/Ctc1, Stn1, Ten1). The focus of this review is on the CST complex and its role in telomere maintenance. Although initially thought to be unique to yeast, it is now evident that the CST complex is present in a diverse range of organisms where it contributes to genome maintenance. The CST accomplishes these tasks via telomere capping and by regulating telomerase and DNA polymerase alpha-primase (polα-primase) access to telomeres, a process closely coordinated with the shelterin complex in most organisms. The goal of this review is to provide a brief but comprehensive account of the diverse, and in some cases organism-dependent, functions of the CST complex and how it contributes to telomere maintenance and cell proliferation.
Highlights
Telomeres compose the non-coding ends of eukaryotic chromosomes and play a crucial role in the protection and replication of our genome [1,2]
Shelterin is a six subunit complex consisting of TRF1, TRF2, TIN2, RAP1, POT1, TPP1, and localizes to double- and single-stranded telomeric DNA (Fig. 1) [11]
There is still a lot to learn about the role of shelterin at telomeres, work from a confluence of labs has shown that it is critical for suppressing DNA damage response (DDR) at telomeres, preventing chromosome fusions [11]
Summary
Telomeres compose the non-coding ends of eukaryotic chromosomes and play a crucial role in the protection and replication of our genome [1,2]. Telomeres together with telomere binding complexes, such as shelterin, repress unwanted DNA damage response (DDR) and serve as a buffer between essential genomic information and the ends of chromosomes. They promote the full replication of our genome, preventing senescence, which is usually associated with significant telomere shortening [5,6]. CST localizes to the single-stranded telomeric DNA, including the telomeric overhang where it is involved in chromosome end capping and telomere length regulation (Fig. 1) [9,17,18,19,20]. Further insight in the molecular mechanisms of telomere maintenance will allow us to better understand the role of telomere dysfunction in human disease
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