Every living cell contains genetic information in the form of chromosomal DNA. Chromosomes can be circular in prokaryotic, or simpler single-celled organisms such as bacteria, but tend to be linear in more complex eukaryotic cells. The replicon, or the enzymatic complex that replicates DNA has limitations on its efficiency and capabilities. For example, eukaryotic DNA polymerase requires a short RNA primer to begin replication on the lagging strand, because of this replication cannot continue replication all the way to the end of the chromosome, and it has been shown that anywhere between 50 and 150 base pairs are lost from the ends of eukaryotic chromosomes for each round of DNA replication (Kim, et al. 2016). This is problematic, because
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The repeated sequence is TTAGGG and these regions are also associated with proteins that function to stabilize these regions (García-Calzón, et al. 2014). Telomeres are a non-coding region of the DNA, and their main function is to help maintain chromosomal stability, as well as to protect chromosomes from serious complications, such as end-to-end fusions, and degradation (Martens, et al. 2016; Nielsen, et al. 2015; Savela, et al. 2013). Telomeres are not infinite, but they can be regenerated by the enzyme telomerase. Telomerase is active in utero, as well as in some diseased cell types like cancer cells; however, in healthy somatic cells, telomerase is present either in very low levels or is not present at all (Nielsen, et al. 2015). As organisms age and their cells undergo more rounds of replication, their telomeres shorten. This has been confirmed in multiple studies, and in fact, telomere length is widely considered to be a biological marker of aging (Hamad, et al. 2016; Kajantie, et al. 2012; Kim, et al. 2016; Martens, et al. 2016; Nielsen, et al. …show more content…
Senescence is a metabolically active, but non-replicative state of the cell cycle, where the cells are arrested at the G0 stage and senescence has been associated with organismal aging (Nielsen, et al. 2015). Cells that continue to replicate with severely degraded telomeres may be at a higher risk damaging the coding regions of their DNA, or undergoing chromosomal fusions. It comes as no surprise then, that shortened telomeres have been associated with a wide variety of diseases and disorders that are often commonly associated with advanced age, some of these include high levels of oxidative stress, insulin resistance, type 2 diabetes, cardiovascular disease, atherosclerosis, hypertension, osteoporosis, chronic inflammation, hormonal and metabolic disturbances, dementia, Alzheimers’ disease, Parkinson's disease and obesity (Fillman, et al. 2016; Hamad, et al. 2016; Kajantie, et al. 2012; Kim, et al. 2016; Martens, et al. 2016; Nielsen, et al. 2015). In addition to this, in vitro studies have shown that human cells with shortened telomeres have a higher likelihood of developing cellular abnormalities and dysfunctions, entering senescence, or of dying (Hamad, et al.
The repeated sequence is TTAGGG and these regions are also associated with proteins that function to stabilize these regions (García-Calzón, et al. 2014). Telomeres are a non-coding region of the DNA, and their main function is to help maintain chromosomal stability, as well as to protect chromosomes from serious complications, such as end-to-end fusions, and degradation (Martens, et al. 2016; Nielsen, et al. 2015; Savela, et al. 2013). Telomeres are not infinite, but they can be regenerated by the enzyme telomerase. Telomerase is active in utero, as well as in some diseased cell types like cancer cells; however, in healthy somatic cells, telomerase is present either in very low levels or is not present at all (Nielsen, et al. 2015). As organisms age and their cells undergo more rounds of replication, their telomeres shorten. This has been confirmed in multiple studies, and in fact, telomere length is widely considered to be a biological marker of aging (Hamad, et al. 2016; Kajantie, et al. 2012; Kim, et al. 2016; Martens, et al. 2016; Nielsen, et al. …show more content…
Senescence is a metabolically active, but non-replicative state of the cell cycle, where the cells are arrested at the G0 stage and senescence has been associated with organismal aging (Nielsen, et al. 2015). Cells that continue to replicate with severely degraded telomeres may be at a higher risk damaging the coding regions of their DNA, or undergoing chromosomal fusions. It comes as no surprise then, that shortened telomeres have been associated with a wide variety of diseases and disorders that are often commonly associated with advanced age, some of these include high levels of oxidative stress, insulin resistance, type 2 diabetes, cardiovascular disease, atherosclerosis, hypertension, osteoporosis, chronic inflammation, hormonal and metabolic disturbances, dementia, Alzheimers’ disease, Parkinson's disease and obesity (Fillman, et al. 2016; Hamad, et al. 2016; Kajantie, et al. 2012; Kim, et al. 2016; Martens, et al. 2016; Nielsen, et al. 2015). In addition to this, in vitro studies have shown that human cells with shortened telomeres have a higher likelihood of developing cellular abnormalities and dysfunctions, entering senescence, or of dying (Hamad, et al.