Aarti Patel<br />Garielle Wagnac <br />Telomeres and Telomerase Lecture<br />Telomeres are regions of uncoded genetic mate...
Telomere paper
Telomere paper
Telomere paper
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Telomere paper


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Telomere paper

  1. 1. Aarti Patel<br />Garielle Wagnac <br />Telomeres and Telomerase Lecture<br />Telomeres are regions of uncoded genetic material found at the ends of chromosomes. They are a repeating sequence of nucleotides that do not code for any type of protein. They function in protection of the genetic material. Telomeres and Telomerase: Implications for Cancer and Diseases of Aging is a lecture about the effect of telomeres on aging and diseases of aging. Elizabeth Blackburn, Ph.D. presents this lecture at the UCSF Mini Medical School Series. She is a professor of biology and physiology at the department of Biochemistry and Biophysics at the University of California, San Francisco. She starts the lecture off with a general statement “Elderly subjects demonstrating exceptional longevity have generally been spared major age-related diseases such as cardiovascular disease, diabetes mellitus, and cancer, which are disease responsible for most deaths in the elderly.” She says, “If we care about age and aging, then we should also care about what cause the most deaths.” She explains how telomeres play an important role in protection of chromosomes. She explains how they are important to aging and diseases. She says age depends on two factors: environmental and genetic.<br />Dr. Elizabeth Blackburn starts off the lecture by introducing telomeres. She gives a brief definition of telomeres. Telomeres protect the genetic material at the end of DNA. Dr. Blackburn refers to aglet as an example. She compares how the aglet protects the ends of the shoe laces from fraying the way the same way the telomeres protect the DNA from being lost and the chromosomes becoming smaller. They also serve as a landing pad for particular proteins that protect the DNA and form a big sheath around it. Dr. Blackburn emphasizes how without telomeres the daughter cells would become shorter and shorter. <br />She poses the question as to how we age. Dr. Blackburn informs on the 3 major causes of death. They are the following: cardiovascular disease, diabetes, cancer. We then discover the meaning behind her the research she has done. How do we age and what affects it? Is it due to environmental factors, genetics, or both? She connects telomeres and telomerase to this ubiquitous question. <br />Before she discusses the connection of telomeres and aging, she presents a study done by Lover and Loft. They focused on 5,779 adult daughters from the same economic status, racial group and well kept records. The women studied were over 30 years old. They focused on the parents’ lifespan and compare to the daughter’s lifespan. Men weren’t used because their death was caused too many non-health and environmental reasons, such as war. The study showed that if the mother lived to be 85 or older then the daughter will live longer. The mother’s lifespan is directly proportionate to the daughter’s life span. This data shows that genes do have an impact on age. However, if the mother’s life span didn’t live past 85 then the studies showed that the daughter’s lifespan could not be predicted. It is hypothesized that it is caused by other environmental factors. The father’s age was very influential if they lived past 75. This study showed that genetics are not an overwhelming factor in aging unless the parents live pasta certain age. The study by the two scientist help progress the lecture into what else factors into aging. <br />Dr. Blackburn shows a video explaining the role of telomerase in the maintenance of telomeres. This video uses music strips as the DNA. The notes represent the nucleotides of the DNA strands. The video starts by explaining what happens when cells divide. It explains the fact that the chromosomes become shorter after each replication. The DNA polymerase “falls off” before it reaches the end. Due to this, the chromosomes shorten every time they replicate. Then cells eventually stop dividing. To maintain the length of the chromosome and allow the cell to keep dividing, telomerase adds extra nucleotides to the ends of chromosomes. When DNA polymerase replicated, the chromosome would not significantly shorten.<br />Telomerase is the next topic and we see that it affects our cells and DNA immensely. Dr. Blackburn explains how telomerase maintains the telomeres. It adds on the repeated sequence segment (TTAGGG) onto the existing telomeres to make the telomere as a whole longer and not diminish. The telomere sequence is specified by telomerase. This enzyme can be beneficial but also has a downside. Because, its function is to continue to add telomeres and that is a huge cancer promoter. Cancer cells go rampant which affects telomeres. The telomeres do not know when to stop. When telomerase is removed from cancer cells they react adversely. The cancer cells stopped replicating as fast as they used to. With this being stated, you can see that the cells are “addicted” to telomerase. Dr. Blackburn devises a way for cancer cell addiction to telomerase to work against them. This experiment is brilliant. In the experiment, the sequence that telomerase adds onto the telomere would be altered. Some of the bases would be a change in the telomere repeating sequence. This change would affect how the protective proteins bind. The protective proteins actually would not bind to the tops of the telomeres because they do not have an affinity for the sequence. Once the protective proteins can not bind to the telomeres then when DNA replication takes place the telomeres will continue to get shorter until they diminish and we lose DNA. The change in the telomere sequence caused for many of the cancer cells died. This is experiment is one of the ways that we could attack cancer cells. <br />Telomerase also has a positive function. It replenishes the healthy body cells and protects the telomeres. Stem cells have an abundance of telomerase because they are always dividing. It is necessary for these cells to be constantly dividing all throughout life. For example, stem cells for blood or immune system need to keep dividing in order to provide blood for the body. Constant activation of telomerase, in this case, is beneficial for the body. It would keep a homeostatic balance in telomere length when these cells are constantly dividing. However, telomeres are gradually shortening throughout life. The shortening rate of telomeres is not uniform. Most of the shortening is done at a very young age. A rare disease, caused by a nonfunctional telomerase gene, can cause bone marrow failure and young death in humans. Of the two genes for telomerase, a daughter cell receives, if one is defective or mutant, full telomerase activity is not acquired. This concludes that cells require both genes for proper telomerase activity. This disease shortens telomere lengths as well. In an experiment, chromosomes were divided without telomeres. At a certain telomere length, the cells were unable to divide. Another set of chromosomes were divided with a small amount of telomerase. They cells continued to dived, even with a shorter telomere. They were stable at a shorter telomere length then the first set. This concluded that telomerase also stabilizes short telomeres.<br />One study took a random group of elderly people and compared their mortality to their telomere length. It found that those with shorter telomeres had a high mortality rate and were more susceptible to age related diseases. Dr. Blackburn questioned whether it was the telomere length that made those people more susceptible or was is that the people had been fighting a disease off for a long time, therefore causing telomeres to shorten. She and her team found a beginning to the answer. This study looked at telomere maintenance and psychological stress. A group of healthy middle aged women who where biological mothers, were observed. Some mothers had a healthy child and others had a chronically ill child. The stress levels of all the mothers taken by questionnaire. The higher the score was, the higher their stress level was. The collaborators wanted to find out whether or not stress levels and caregiving durations were related to cell aging markers. They found that those with high stress levels had lower telomerase activity, then those with low stress levels. High stress groups also had more telomere shortening. Oxidative stress levels were high in those with high stress levels. This shows that there is a link between DNA maintenance and stress levels. The number of years of caregiving also affected the telomerase activity, telomere length, and oxidative stress. This now shows that there is a link between the brain and telomere maintenance. This study concluded that low telomerase activity was associated with the major factors of cardiovascular disease.<br />