Devil Facial Disease

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

The length of the telomere indicates age-related diseases, unhealthy lifestyle, and longevity in the lifespan.

Restriction enzymes cut DNA at certain sites to create multiple DNA fragments. Restriction enzyme HindIII has known DNA fragment lengths and recognition sites when digesting lambda DNA, while the lambda DNA recognition site for restriction enzyme XhoI is unknown. The goal of this study is to determine the lambda recognition site of XhoI by comparing a HindIII digest and a HindIII and XhoI double digest on an electrophoresis gel. The HindIII digest had a band at 9.4 kb, but this band was not visible in the double digest, therefore we concluded the recognition site for XhoI was around 9.4kb. There were also two additional DNA

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.

Telomerase (or terminal transferase) is an enzyme made of proteins, specifically reverse transcriptase (Telomerase Reverse Transcriptase-TERT), and RNA subunits. Nonetheless, chicken TERT (chTERT) shares 45% amino acid identity with human TERT (hTERT). However, chTERT is larger than the hTERT because of an extensive N-terminal flexible linker region. Also, chTERT is found on chromosome 2q21 near an interstitial telomere site. Generally, the role of this enzyme is to elongate the end of chromosomes by adding the repeated base sequence of TTAGGG, as described above. This enzyme can be found in fetal tissue, germ cells, and tumor cells. Telomerase activity is critical high on development because of the continued growth and division of the cells.

Devil Facial Tumor Disease (DFTD) can be recognized by lumps around the face and neck.

Tasmanian devil (Sarcophilus harrisii) populations on the island of Tasmania have experienced a rapid decline during the past twenty years due to the spread of a cancer called Devil Facial Tumor Disease or DFTD. DFTD is a deadly contagious cancer that is characterized by red oozing lesions or tumors that form on the face and mouth of the Tasmanian devil. The cancer spreads from one devil to another when a DFTD infected devil bites a healthy devil thereby infecting the open wounds with cancer cells. Once contracted the devil dies within six months due to infection or starvation because the tumors in mouth hinder feeding. However, researches lead by biologist Andrew Storfer have discovered that some Tasmanian devil populations have evolved a

Malignancies, pulmonary fibrosis, and liver cirrhosis, other signs, could be developed for patients with dyskeratosis. in a similar way proved that can be used as a special diagnostic marker for scan of a large, nonconsanguineous and also with no mutations in DKC1, TERC, or TERT. Autosomal forms of dyskeratosis congenita are formed because of mutations in TERT, TERC, NHP2, NOP10 the last two are proteins associated with the telomerase complex and their mutations are discovered in autosomal recessive cases, or TINF2 these mutations cause telomere shortening by telomerase complex or, while, TINF2, lead to deprotection of telomeres.

Targeting these Telomere/Shelterin compounds may be useful to suppress the tumour cells, killing it off.Grueber CE et al. 2015

Hello Amy. I enjoyed reading your post. Individuals with telomere disorder have shorter telomeres for their age. One example of telomere disorder is Dyskeratosis congenita. This disorder caused by a mutation of TERT, TERC, DKC1 or TINF2 genes. Affected individuals have multiple medical problems affecting the nails, oral mucosa, and skin. They are also high risk of developing life-threatening conditions such as cancer and bone marrow failure. “Increasing telomerase levels ought to lengthen telomeres but in the case of cancer, too much telomerase can be just as bad as too little telomeres” (Rehman, 2014). Telomerase could slow down the aging process, but it could also increase the risk of developing cancer. Great job Michaela

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

The disease was discovered to be spread as an allograft (a tissue graft between non-identical members of the same species) between the Devils after genetic sequencing revealed that tumours from different individuals contained identical anomalies in the chromosomal arrangement, too complex to have

Throughout the past years, research of this unexpected instability has created a number of surprising discoveries. As a matter of fact, it has led to the findings of a great enzyme named telomerase that acts on telomeres and is thought to be required for the maintenance of many human cancers. Telomerase, the ends of the chromosomes, are eukaryotic ribonucleoprotein complex, which contains both an essential RNA and a protein reverse transcriptase subunit. They are meant to protect the chromosomal ends. They basically cap the ends of the chromosomes, thus protecting the ends. Unlike viral or retroviral reverse transcriptase’s, like the ones on HIV-1, the cellular enzyme telomerase focuses in making the multiple short tandem repeats that are at

The cell is busier than the streets of New York, and when it splits, it must have everything go perfectly. If the chromosomes were to break down, the DNA it is holding could be damaged. That could be catastrophic for the cell. This is where telomere comes in. Telomere is a small area of nucleotides that repeat at the end of every chromosome to keep the chromosome from falling apart and breaking down. But, the telomere doesn’t just appear out of nowhere. It is created just like everything else, with DNA. Nobel Prize winner cell biologist Carol W. Greider discovered the enzyme telomerase. Telomerase is what creates the DNA found in telomere.

Time is of the essence! By the end of this research paper the reader will know the reasoning behind time itself. A telomere is quite significant because it can detect cancer, diseases, and aging. The telomer was discovered around the 1960’s by Dr. Leonard Hayflick he discovered it by learning about how long a cell can live. There are billions of cells through plants, animals, and humans it’s how an organism operates. A telomer is at the end of each chromosome inside a eukaryote cell (Plant and Animal Cell) and its importance is copying DNA (Deoxyribonucleic Acid). DNA is the genetics that we obtain through our parents. If we could preserve the telomer to be continuous then organisms can become eternal. A telomer holds the true meaning of