Shorter telomeres can be transmitted epigenetically to offspring | Elissa Epel
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Accelerated aging syndromes, such as Werner syndrome and Hutchinson-Gilford progeria syndrome, are characterized by genetic mutations that promote increased DNA damage, particularly at telomeres. These conditions, which lead to premature aging and an increased risk of cancer, cardiovascular disease, and metabolic disorders, are hereditary. In this clip, Dr. Elissa Epel explains how these aging syndromes – as well as other factors that affect telomere length – can also be passed to offspring via epigenetic mechanisms.
Rhonda: And there are some human diseases where telomeres are short and that does have a progeria type of effect, like Werner.
Elissa: Right. So that's super interesting. So in this certain handful of genetic disorders, where people might have half a dose for telomerase, so their telomeres shorten quickly, they develop diseases that are... You know, the diseases of bone marrow, they don't have enough white blood cells or these, you know, lung diseases. And so what is interesting about that is we know in those cases that it's the telomerase and the short telomeres that are causing this early aging. And they can transmit, you know, the mutated gene to offspring and they get the aging syndrome. They also can transmit just the short telomeres epigenetically, like in a direct epigenetic way...
Rhonda: That's interesting.
Elissa: To the offspring. So the offspring may, thank goodness, not get the mutated gene but they still get short telomeres. And they might have a mild aging syndrome from that. So that's something new that we know from these genetic disorders that might happen in us, too. We might be epigenetically transmitting short telomeres directly to our offspring, whether we have a gene for that or not, just based on what our telomeres are.
Genetic control elicited by factors other than modification of the genetic code found in the sequence of DNA. Epigenetic changes determine which genes are being expressed, which in turn may influence disease risk. Some epigenetic changes are heritable.
An extremely rare genetic disorder in which symptoms resembling aspects of aging are manifested at a very early age. People born with progeria typically live to their mid teens to early twenties. Although the term progeria applies strictly speaking to all diseases characterized by premature aging symptoms, it is often applied specifically in reference to Hutchinson–Gilford progeria syndrome (HGPS).
An enzyme that extends the telomeres of chromosomes. Telomerase adds specific nucleotide sequences to the ends of existing chromosomes. Telomerase activity is highly regulated during development, and its activity is at an almost undetectable level of activity in fully developed cells. This lack of activity causes the cell to age. If telomerase is activated in a cell, the cell will continue to grow and divide, or become "immortal," which is important to both aging and cancer. Telomerase enzyme activity has been detected in more than 90 percent of human cancers.
Distinctive structures comprised of short, repetitive sequences of DNA located on the ends of chromosomes. Telomeres form a protective “cap” – a sort of disposable buffer that gradually shortens with age – that prevents chromosomes from losing genes or sticking to other chromosomes during cell division. When the telomeres on a cell’s chromosomes get too short, the chromosome reaches a “critical length,” and the cell stops dividing (senescence) or dies (apoptosis). Telomeres are replenished by the enzyme telomerase, a reverse transcriptase.
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Telomeres News
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