Embryo Project Encyclopedia

Telomeres are sequences of DNA on the ends of chromosomes that protect chromosomes from sticking to each other or tangling, which could cause irregularities in normal DNA functions. As cells replicate, telomeres shorten at the end of chromosomes, which correlates to senescence or cellular aging. Integral to this process is telomerase, which is an enzyme that repairs telomeres and is present in various cells in the human body, especially during human growth and development. Telomeres and telomerase are required for normal human embryonic development because they protect DNA as it completes multiple rounds of replication.

Carol Widney Greider studied telomeres and telomerase in the US at the turn of the twenty-first century. She worked primarily at the University of California, Berkeley in Berkeley, California.
She received the Nobel Prize in Physiology or Medicine in 2009, along with Elizabeth Blackburn and Jack Szostak, for their research on telomeres and telomerase. Telomeres are repetitive sequences of
DNA at the ends of chromosomes that protect chromosomes from tangling, and they provide some protection from mutations. Greider also studied telomerase, an enzyme that repairs telomeres. Without telomeres, chromosomes are subject to mutations that can lead to
cell death, and without telomerase, cells might not reproduce fast enough during embryonic development. Greider's research on telomeres helped scientists explain how chromosomes function within cells.

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.

When cells-but not DNA-from two or more genetically distinct individuals combine to form a new individual, the result is called a chimera. Though chimeras occasionally occur in nature, scientists have produced chimeras in a laboratory setting since the 1960s. During the creation of a chimera, the DNA molecules do not exchange genetic material (recombine), unlike in sexual reproduction or in hybrid organisms, which result from genetic material exchanged between two different species. A chimera instead contains discrete cell populations with two unique sets of parental genes. Chimeras can occur when two independent organisms fuse at a cellular level to form one organism, or when a population of cells is transferred from one organism to another. Chimeras created in laboratories have helped scientists to identify developmental mechanisms and processes across species. Some experiments involving chimeras aim to provide further knowledge of immune reactions against disease or to create animal models to understand human disease.

The Hayflick Limit is a concept that helps to explain the
mechanisms behind cellular aging. The concept states that a normal human
cell can only replicate and divide forty to sixty times before it
cannot divide anymore, and will break down by programmed cell death
or apoptosis. The concept of the Hayflick Limit revised Alexis
Carrel's earlier theory, which stated that cells can replicate
themselves infinitely. Leonard Hayflick developed the concept while
at the Wistar Institute in Philadelphia,
Pennsylvania, in 1965. In his 1974 book Intrinsic
Mutagenesis, Frank Macfarlane Burnet named the concept after
Hayflick. The concept of the Hayflick Limit helped scientists study
the effects of cellular aging on human populations from embryonic
development to death, including the discovery of the effects of
shortening repetitive sequences of DNA, called telomeres, on the
ends of chromosomes. Elizabeth Blackburn, Jack Szostak and Carol
Greider received the Nobel Prize in Physiology or Medicine in 2009
for their work on genetic structures related to the Hayflick
Limit.

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.

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.