Henrietta Laks Lab Report

In order to appreciate the function of TPP1, POT1’s function must be understood. The main function of POT1 is to recognize and bind ssDNA. Indeed, TPP1-PBD interacts with POT1. Indeed, TPP1 is the responsible protein of recruiting the POT1to the ss telomeric DNA. In fact, data presented suggest that the TPP1-PBD is the main reason of the POT1 recruitment and interaction to the telomeric DNA [18]. The deletion of TPP1 interaction domain in the POT1, POT1 is not recruited to the telomeric DNA. Similarly, knocking down the TPP1 results in inhabitation of the POT1 recruitment. These data prove that TPP1 is responsible for the recruitment of the telomere.

Elizabeth Blackburn is an amazing woman; who comes from a family of physicians. She has always had a passion for animals and science; she found biology to be her favorite subject in school. She was fascinated by the visual impacts of science through books. Perhaps, it is her enthusiasm for biology that inspired her to be one of the leading biochemists today. Elizabeth helped in the discovery of “the fountain of youth.” Elizabeth and two of her colleagues discovered a way for chromosomes to be copied during cell division. Within this discovery, they also found a unique DNA sequence in the telomeres that protects these cells against degradation. In 2009, Dr. Blackburn was awarded the Nobel Prize in Medicine.

Telomeres make up the tips of linear chromosomes and function to protect and stabilize the chromosomes from degradation (Pierce 2014). There are other functions, but the primary one is protection. At each replication, DNA shortens by just a few base pairs due to the nature of replication in eukaryotes (who have linear chromosomes). The two strands of DNA are synthesized at different rates, creating a leading strand and a lagging strand. The leading strand is replicated quickly and fluidly in a 5’ to 3’ direction, as seen in Image 1. The lagging strand is replicated in a backstitch patter. Primers are placed along the DNA strand and DNA polymerase replaces them with segments of DNA. It can only do this, though, if a 3’-OH group is present. The 3’-OH group precedes the primer, and would sit just to the right of the green primers in Image 1. No 3’-OH group would be present at the end of the chromosome because it only exists on one side of the primer. The area where the primer is sitting would not be replicated, and thus the DNA would shorten. Tandem sequences of noncoding DNA sit at the ends of the

Telomerase (TERT) is an enzyme responsible for maintaining the ends of telomeres and reversing the process of telomere shortening in humans by adding a “TTAGGG” polynucleotide to the 3’ end of the telomere. The addition of the “TTAGGG” compensates for inefficiencies in replication of the ends of DNA in eukaryotes. Telomerase is limited to highly proliferative cells such as germ cells and lymphocytes where the telomerase is necessary to maintain telomere length, and the telomeres themselves are not sufficiently long to facilitate such rapid cell division without incurring damage to the DNA. Most somatic cells exhibit no telomerase activity and in cells where telomerase is present telomerase activity is strictly regulated. In cells that exhibit

Scientist have the discovered the interactions between molecules and proteins within the cell that inhibit or stop the body’s ability to repair DNA damage over time. As the body ages, its ability to repair DNA gradually declines and that loss leads to bodily degeneration and a higher risk for cancer, the uncontrolled and abnormal growth of cells that don’t undergo apoptosis or cell death. This discovery is important to the scientific and medical community because it identifies the main players in the protein bindings and molecules that inhibit or promote DNA repair within the cells. This is important because with the key mechanism of cellular degeneration and aging being discovered, medical researchers can develop therapeutic techniques to

Carol W. Greider is a cell biologist who has discovered the enzyme telomerase in 1984 which she won the nobel prize award. Greider pioneered research on the structure of telomeres, the ends of the chromosomes. She works in a lab which can work with DNA bases to the ends of chromosomes. The thesis she made was “The identification of a specific telomere terminal transferase activity in Tetrahymena extracts.”

In current society, cancer is one of the most fatal and prevalent diseases to exist. However, new research being conducted on telomeres and telomerase provides insight on not only the aging process and mortality of cells, but also on how the idea of cell death connects to cancer cells. By gaining knowledge on the supposed immortality of cancer cells, researchers are acquiring a higher understanding of the subject, and attempting to work on alternate techniques to provide treatment for the illness. The connection between telomeres and cancer and the momentous discoveries being made on them is revolutionizing the world through potential current and future applications that have significant implications for cancer treatment, and society, the

The specific aim of the project is original as no detailed reference values for telomere length in children are available. However, the probable impact of the reference values will be low because telomere length is a biomarker of questionable value. The association of telomere attrition with mortality and morbidity has been widely reported, but it has many limitations. An important limitation is the technical variability and dependence on laboratory procedures. It is important to remark that the project aims to determine telomere length with qPCR, a method of known sensitivity to differences in technique or equipment. Therefore, the reference values will be of limited validity beyond the specific laboratory where they are developed. In addition,

Carol W. Greider was born in San Diego on april 15 1961.(54 years old).She hasn’t died and she's a bloomberg distinguished professor. she discovered enzyme telomerase in 1984 one year Greider then completed her postdoctoral work, and also held a faculty position, at the Cold Spring Harbor Laboratory, Long Island, New York. During this time, Greider, in collaboration with Ronald A. DePinho, produced the first telomerase knockout mouse, showing that although telomerase is dispensable for life, increasingly short telomeres result in various deleterious phenotypes, colloquially referred to as premature aging. In the mid-1990s, Greider was recruited by Michael D. West, founder of biotechnology company Geron (now CEO of BioTime) to join the company's

Telomerase extends the telomeres of the chromosomes, and it is important during the development period. Although, telomerase activates in 90% of tumors. The function of the enzyme telomerase is when the enzyme extends the telomeres of the chromosomes. The enzyme is making the DNA using RNA as a template (Telomeres and Telomerase). The binding of the enzyme goes to a special RNA molecule to contain a sequencing which is complementary to the telomere repeat. It then extends an overhanging strand of the telomere DNA using the complementary RNA as a template. The overhang then becomes long enough, and the matching strand is made by a normal DNA replication. This finally produces a double-stranded DNA.

In particular telomere length has become a required biomarker for anyone analyzing the effect of and variables into human fitness. Telomere length has been related to obesity, bone demineralization and other aging indexes, including high risk of premature death and development of cancer. It has been found believable that the presences of short telomeres trigger cell senescence in vivo, in consequence affecting organ and tissue function. Their observation strongly support that telomere shorting is a major cause of cell senescence in organs with high proliferative potential, detectable in aged human individuals. Which causes the degeneration of organs and bones that lead to the age related diseases that are shorting the lifespan of humans. Telomere length has become an excellent predictive measure for some of these age related disease because of its close correlation to the

Human chromosomes are incredibly complex, containing a variety of different structures necessary to maintain its function; one of these is called a Telomere and is found at the ends of the chromosomes. Telomeres contain thousands of repeats of the repetitive TTAGGG DNA sequence; this is combined with a complex enzyme known as telomerase. Furthermore, the function of this ribonucleoprotein enzyme complex is to maintain telomere length in cancer cells by adding TTAGGG repeats onto the telomeric ends of the chromosomes; this compensates for the normal expected shortening of telomeres which occurs in all dividing cells.

During each and every cell replication, chromosomes shrink by a small, but noticeable amount. Because of this, telomeres cap the ends to protect the coding regions of the chromosomes. With each generation of DNA, more and more of the telomere disappears. An enzyme slowly rebuilds them, but it cannot keep up with the degradation during chromosome replication. Eventually the shortened telomeres cause the cell to go through apoptosis (Pierce 2014). Because telomeres are one cause of cell death, it is hypothesized that telomere size can determine the health and age of an individual. Research has shown a correlation between telomere length and chronic disease. Those with chronic diseases usually have significantly shorter telomeres. This raises the questions of what the correlation means. Chronic disease could shorten the telomeres, or short telomeres could cause chronic disease. Another hypothesis exists that shortened telomeres and chronic disease are both caused by another force; they occur simultaneously, but one does not necessarily cause the other. Researchers have also seen a correlation between telomere length and age. Physical age may be derived from the number of cells that have undergone apoptosis. There are a number of things that we can do to prevent telomere reduction. Diet and exercise both play a key role in this. Things that are “bad” for us, such as smoking and stress, increases the rate at which telomeres shorten. By

DNA replication results in the gradual shortening of telomeres over time, leading to the activation of senescence or apoptosis. Therefore, telomere length is a key biological signal to limit the indefinite proliferation of somatic cells (Roumelioti, et al., 2016). However, cancer cells can overcome telomere shortening by synthesising a new telomeric DNA from an RNA template through the expression of telomerase (Roumelioti, et al., 2016). Alternatively, 10-15% of human cancers utilise a DNA template in a homology-directed synthesis mechanism called alternative lengthening of telomeres (ALT) (Cesare & Reddel, 2010). However, the process by which DNA damage such as telomeric shortening results in the execution of homology-directed synthesis,

Telomeres are terminal sequences of genomic DNA. They are important for the stability of chromosomes. Centromeres are sequences located in centers of chromosomes. They are important for chromosome stability and cell division.