Teloomerase Lab Report

Instead of losing telomeres after each reproduction, the cells replenish, or lengthen, the telomeres using an enzyme called telomerase.

Introduction: The biological membranes are composed of phospholipid bilayers, each phospholipid with hydrophilic heads and hydrophobic tails, and proteins. This arrangement of the proteins and lipids produces a selectively permeable membrane. Many kinds of molecules surround or are contained within

The oxidation number of an atom of any free element is ZERO. Means to say there is only one kind of atom present, no charge.

Telomerase is able to add DNA nucleotides to the ends of telomeres (the end of DNA sequences). After replication, a small amount of the telomeres are cut off. When the telomeres are cut too many times, the cell has met its Hayflick limit. It is believed that when an individuals cells have divided too many times, that they die.

As our cells divide and our DNA replicates, our telomeres provide a start and an end point for the enzyme DNA polymerase to attach to our chromosomes and replicate our DNA. By using a repeated, non-coding section of DNA as the starting point for this replication, the telomeres allow our cells to replicate without damaging important genes at the attachment point of the replicating enzyme. As this occurs though, our telomere begin to lose base pairs

A normal cell will use the genetic information that is found in its DNA, following it’s directions to build proteins. Cells will splice together segments of genetic information, called exons which contain the directions for building proteins. The cells also remove any letters of unused genetic information, called introns. This process is called RNA splicing and it appears to be altered by telomere shortening and this in turn negatively affects the building of proteins that are important in a cell’s cytoskeleton. The cytoskeleton is the internal framework, or scaffolding of a cell, which keeps the cell from collapsing.

Telomere length may be normal, despite a strong suspicion primarily based on the clinical findings. As yet unidentified genes that have an effect on telomerase expression would possibly mildly impair telomere repair or have off-target pathologic

A Molisch's test requires mixing the test solution with Molisch's reagent. One prepares this reagent by dissolving alpha-naphthol in 95 percent ethyl alcohol. After mixing the test solution and reagent, the individual adds 2 milliliters of the test solution to a test tube and pours 2 milliliters of sulfuric acid down the side of the slanted test tube without mixing. The mineral acid is very heavy, so it forms a bottom layer.

Secondly, the knowledge of this link led to significant implications and applications for cancer treatment, which are highlighted through recent and important discoveries. First of all, current methods of cancer treatment are unreliable; both chemotherapy and radiotherapy have dangerous side effects, including second cancers12, 13. As a result, vigorous research is being conducted in using the connection between telomeres and cancer to treat the illness. One potential solution that scientists discovered is the use of telomerase inhibitors, which would actively inhibit the enzyme10. An experimental anticancer technique that Geron researchers tested is a mixture of the drug Alkeran and an anti-telomerase agent GRN163L10. The drugs hindered the development precancerous cells, and even fought real cancers10. In another experiment, scientists inhibited telomerase activity in a cancer by building complementary RNA strands of the telomerase production gene, which would attach to the telomerase mRNA and obstruct the process9. The

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.

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.

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,

Nuclear transfer was used to generate transgenic pigs that expressed the N-terminal region of mutant HTT (including 1–208 amino acids) composed of 105 repeats of glutamine residue. Among the five piglets, three of them died after 3 days of birth and the fourth died after 25 days. Only one offspring remained alive that did not show any pathological signs at four months of age. The mHTT expression levels was markedly different between piglets [41]. Generation of HD animal models using random intra genomic insertion of the mutant HTT may lead to function disrupting of the other neighbor genes. The destruction of these genes may influence the phenotypes caused by mHTT or may result in a lethal mutation before the manifestation of desired phenotype [43].

Interaction of TRF2 with another shelterin component RAP1 at telomeres has been reported 53,54. Interestingly, RAP1 was also reported to mediate gene regulation through binding to extra-telomeric sites 54,55.