Experiments conducted by Elizabeth Blackburn, Carol Greider, and Jack Szostak from 1982 to 1989 provided theories of how the ends of chromosomes, called telomeres, and the enzyme that repairs telomeres, called telomerase, worked. The experiments took place at the Sidney Farber Cancer Institute and at Harvard Medical School in Boston, Massachusetts, and at the University of California in Berkeley, California. For their research on telomeres and telomerase, Blackburn, Greider, and Szostak received the Nobel Prize in Physiology or Medicine in 2009. Telomeres and telomerase affect the lifespan of mammalian cells and ensure that cells rapidly develop within developing embryos.

Telomerase is an enzyme that regulates the lengths of telomeres in the cells of many organisms, and in humans it begins to function int the early stages of embryonic development. Telomeres are repetitive sequences of DNA on the ends of chromosomes that protect chromosomes from sticking to each other or tangling. In 1989, Gregg Morin found that telomerase was present in human cells. In 1996, Woodring Wright and his team examined human embryonic cells and found that telomerase was active in them. Scientists manipulate telomerase in cells to give cells the capacity to replicate infinitely. Telomerase is also necessary for stem cells to replicate themselves and to develop into more specialized cells in embryos and fetuses.

Telomeres are structures at the ends of DNA strands that get longer in the DNA of sperm cells as males age. That phenomenon is different for most other types of cells, for which telomeres get shorter as organisms age. In 1992, scientists showed that telomere length (TL) in sperm increases with age in contrast to most cell of most other types. Telomeres are the protective caps at the end of DNA strands that preserve chromosomal integrity and contribute to DNA length and stability. In most cells, telomeres shorten with each cell division due to incomplete replication, though the enzyme telomerase functions in some cell lines that undergo repetitive divisions to replenish any lost length and to prevent degradation. Cells, and therefore organisms, with short telomeres are more susceptible to mutations and genetic diseases. While TL increases in a subset of sperm cells and longer telomeres may prevent early disintegration of DNA, it may also prevent natural mechanisms of apoptosis, or cell death, from occurring in abnormal sperm.