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Telomeres at the end of a chromosome. The relationship between telomeres and longevity and changing the length of telomeres is one of the new fields of research on increasing human lifespan and even human immortality. [1] [2] Telomeres are sequences at the ends of chromosomes that shorten with each cell division and determine the lifespan of ...
Normal aging is associated with telomere shortening in both humans and mice, and studies on genetically modified animal models suggest causal links between telomere erosion and aging. [10] Leonard Hayflick demonstrated that a normal human fetal cell population will divide between 40 and 60 times in cell culture before entering a senescence phase.
Critically short telomeres trigger a DNA damage response and cellular senescence. [32] Mice have much longer telomeres, but a greatly accelerated telomere shortening-rate and greatly reduced lifespan compared to humans and elephants. [33] Telomere shortening is associated with aging, mortality, and aging-related diseases in experimental animals.
Their longevity may be due to telomerase, an enzyme that repairs long repetitive sections of DNA sequences at the ends of chromosomes, referred to as telomeres. Telomerase is expressed by most vertebrates during embryonic stages but is generally absent from adult stages of life. [ 23 ]
Longer-lived species possess many mechanisms for offsetting damage due to causes such as oxidation, telomere shortening, and other deteriorative processes. Shorter-lived species, having earlier ages of sexual maturity, have less need for longevity and thus did not evolve or retain the more-effective repair mechanisms.
As the cell divides, the telomeres on the end of a linear chromosome get shorter. The telomeres will eventually no longer be present on the chromosome. This end stage is the concept that links the deterioration of telomeres to aging. Top: Primary mouse embryonic fibroblast cells (MEFs) before senescence. Spindle-shaped.
This phenomenon is not only seen in yeast, but has also been seen in aging worms, during aging of human diploid primary fibroblasts, and in senescent human cells. In human primary fibroblasts, reduced synthesis of new histones was seen to be a consequence of shortened telomeres that activate the DNA damage response. Loss of core histones may be ...
They then used α factor to block cells with induced short telomeres in late G1 phase and measured the change in telomere length when the cells were released under a variety of conditions. They found that when the cells were released and concurrently treated with nocodazole , a G2/M phase cell cycle inhibitor, telomere length increased for the ...