Research Paper on Effects of Telomeres on Mammalian Life History

Introduction

Most organisms are exposed to external environmental stressors at different circumstances in life, and the responses to the stressors have been enhanced by evolution to offer the best results. Exposure to stress accelerates the rate of telomere degradation. It is anticipated that the environmental changes shall substantially upsurge prolonged stress exposure in a majority of animal groups in the forthcoming years. The key challenges facing biologists is to comprehend and forecast how the effects of stress influence human, populations, and the ecosystems, and the time expected for the impact to occur. To give the most relevant results on this research, a multi-disciplinary approach of linking the studies on mechanisms with the investigations of fitness significances for people and their progenies is appropriate. One most essential course that has been identified recently is the effects of telomeres dynamics on life longevity. Majority of the studies have been done using mammals, especially humans. The development of organisms is a program that is sternly regulated, where the controlled gene expression assures the formation of a specific phenotype. Telomeres are discrete structures that comprise of short, recurrent sequences and the end of eukaryotic chromosomes. In vertebrates, the telomeres are consist of hundreds of TTAGGG tandems replications that cap the chromosome ends and inhibit them from the degradation of the DNA and also prevents the chromosome from unnecessary repairing. However, the length of the telomeres reduces with age. This indicates that younger mammals have a longer lifespan compared to the old ones. The paper shall discuss the effects of the telomere on the life history of mammals basing the concepts on the length of the telomere.

Is your time best spent reading someone else’s essay? Get a 100% original essay FROM A CERTIFIED WRITER!

Order now

Evolution biology elucidates the outstanding diversity amid organisms in their model of growth, reproduction, and deterioration with age, which are the main characters of life histories. The examination of the distinctions in life history characteristics such as life expectancy and prolificacy divulges negative correlations between these characteristics which are known as tradeoffs of life history. These tradeoffs are apparent in the comparison of different species where there are organisms with a higher reproduction rate and a shorter lifespan. Similarly, individuals also exhibit the same scenario where those that invest too much on reproduction ages quickly. Life history tradeoffs attract specific interests in sections since they pose an underlying problem (Monaghan 2014). The main question is why selection has not concurrently taken full advantage of life history characteristics which led to the evolution of organisms that have prolonged prolificacy and life expectancy which can be described as the 'Darwinian demon.' The explanation of this life history tradeoffs pivots on the results of evolutionary limitations which confident the evolution potential in a way that the traits are not fully exploited. Explaining the nature of the evolutionary restrictions in the life history evolution has been a focus of many researchers in evolutionary biology.

Telomeres may play a significant role in the evolution of the life history tradeoffs of mammals, and ageing which can be founded in the theory of life history which has a parallel concept with the soma theory of ageing and is compatible with the incompatible pleiotropy theory of ageing. The approach of life history identifies that the assortment of achievable evolution results are limited by the definite evolutionary limitations like the need of allocating inadequate resources through numerous competing characteristics including growth, proliferation, and maintenance of somatic mechanisms which retard the continuous accumulation of faults and harms in the body structures (Heidinger et al. 2012). The selection of ideal resource use scheme is expected to result in negative genetic and phenotypic links between some pairs of the life-history characteristics. This methodology instinctively accounts for the presence of tradeoffs stuck between features that are concurrently expressed since the resources put in in one trait cannot be put in in others. This approach also interprets the present -future life history interchanges such as the present reproduction level and future survival or proliferation. Present- next intersections are regularly envisioned to arise since the current venture into reproduction can involve shortages in the venture into sematic maintenance which accelerates the age-related somatic reliability where unless recovered, they can be transferred to the future steps with unfavorable effects on the future survival and reproduction (Blackburn & Epel, 2017). Therefore, the present-future tradeoffs can indicate the senescence course of an organism because of the influences of the present activities on the rate of decline in an age in body cells.

There are various causal roles played by a telomere length in the current, and the future adjustments and ageing stem from a sequence of results that indicate their ability to leave the present activities with adverse effects on the performance in the future. Telomeres help the DNA to repair mechanism to differentiate between a right chromosome ends and a double-stranded break, thus prevents the chromosome from joining together mistakenly. The process of DNA replication is designed in a way that the end of one strand is not wholly duplicated. As a result, this problem may lead to the loss of various essential codes during cell division. The adverse effects of the genome are inhibited by telomeres, which are the end of a chromosome and prevents it from ruin. The telomeric DNA sequence is majorly made of guanine in the compound of six bases. All vertebrates have a similar and all the other eukaryotes. They have been in existence all through the life of human and are highly preserved and effective system of protection of the genome. The DNA of the telomeres usually ends up in a single strand of the TTAGGG sequence, which folds to form a structure that is known as the T-loop (Klegarth, & Eisenberg 2018). Apart from protecting the chromosomes ends from degeneration, telomeres also regulates the segregation of chromosomes during mitosis and meiosis.

Telomere degradation harms future life performance due to the accumulation of disparagingly shortened telomeres in the cells which initiate apoptosis (cell senescence). The continuous loss of telomeric recurrences weakens the shield that covers the chromosome ends in the DNA of a cell. This results in damage in the DNA, which in turn encourages apoptosis. Basing facts on experimental evidence in vitro, telomere degeneration constrains a creative possibility of negative telomerase cells, and the initiation of telomerase expression reestablishes the creative ability while staving-off cellular senescence (Olson et al. 2017). However, researches indicate that even if telomeric mechanisms may be the primary cause of cell senescence in vivo, sometimes the initiation can occur without dependence on the length of the telomere.

Nonetheless, the accumulation of the senescent cells plays a significant part in the reduction of organismal performance due to the related inactive loss of the functions of tissues and their strange secretory shapes. Recent laboratory experiments have been carried out using house mice; the investigation showed that the clearance of senescent cells using various methods counters age related performance. However, telomere induced apoptosis complexes these effects as the replacement of cells through stem cell division is typically expected to fasten stem cell degradation and in turn, leads to stem cell fatigue.

The telomeric sequence shortens during cell division when they become too short such that they are approaching a critical level, the cell begins to deteriorate. At this point, the cells die or remain within a changed profile. The degree of telomere loss in every cell division is higher than the results that are anticipated to occur with the end replication problem. Telomeric DNA is very susceptible to the oxidative damages as compared to the non-telomeric DNA; this is due to the high concentration of guanine and the reduced level of repair in telomeric areas. The redox balance in the cells plays a significant role in the loss rate of the telomere. Consequently, high magnitudes of oxidative destruction have been seen to accelerate the pace of telomere shortening.

Several restoration mechanisms occur and are initiated by the action of the enzyme telomerase, which is capable of replacing the DNA. In mammals and other vertebrates, these enzymes are numerous in the cells that have a high potential of reproduction, for instance, the adult stem and embryonic cells, the basal cells of the epidermis, the male germ line, active lymphocytes, and intestinal crypt cells, as well as the reproductive cells (Klegarth, & Eisenberg 2018). In mammalian early cleavage and mature oocytes, the activity of enzyme telomerase is low. The exercise increases from a blastoderm stage are then slowed down in most body cells after the completion of the embryonic development. Birds and mammals exhibit a similar activity in their embryos. However, scientists have suggested that the telomerase activity varies with the body mass of an organism in mammals.

The length of the telomere gives rise to a mitotic clock that predicts the death of an organism as proposed by various scientists. Degradation of the telomeres occurs naturally with every cell division. However, different lifestyle influences speed up their deterioration, which affects the fitness and health of an organism negatively. Basing the study of the telomere on reproductive ageing in mammals, telomere length varies from males and females. More so, it also varies with the species of the mammal. For instance, the shortening of telomere research done on mice and human indicate that mice do not show substantial ageing of the oocytes. The shortening of the telomere of mice reduces the chiasmata and synapsis while increasing the cell cycle arrest, spindle dysmorphologies, chromosomal abnormalities, and embryo disintegration (Kalmbach et al. 2013). On the other hand, this shortening in women is more significant. These women later produce disintegrated aneuploidy embryos that cannot implant. However, on men, the telomere reserves rejuvenate throughout the lifetime; this explains why men are reproductively viable even at old ages. The difference in the telomere dynamics through the life span of men can be explained by the contrast of the in-born risks of ageing on reproduction amid men and women.

Human exhibit a negative correlation between the length of the telomere and age; however, there is no significant difference in the rates through which the telomeres shorten. The diseases that are most commonly associated with short telomeres include cardiovascular disease. On the other hand, there are environmental factors that can hasten the shortening of the telomeres. Lifestyle habits such as smoking, exercise, and poor diet are the leading accelerators of the process of telomere shortening (Kalmbach et al. 2013). Many diseases are related to the shortening of the telomere, and most are referred to as lifestyle diseases such as diabetes and various cancers.

At this point, it is acceptable that telomere abrasion can have contributory effects in the fate of a cell to the extent that it underwrites to age related reductions in the performance. However, some uncertainties involve the significance of telomere-mediated and telomere-independent mechanisms as seen in the oxidative effects on structures and the tools of telomere that act independently of the length of the telomere (Muraki...