Telome Fusion

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

A new nuclear envelope forms around the separated sister chromosomes. As mitosis completes, cytokinesis is well underway.

These centrioles replicate and the chromosomes line along the equator at metaphase II and spilt at the centromeres causing the chromatids to move to opposite sides at anaphase II. At telophase II the cell divides to form four haploid cells, these are not identical to each other because the cells contains chromosomes from two different parent gametes therefore differ genetically. However, during mitotic division the cells produced are genetically identical to each other because they are produced from the same parent cell. The cell begins to replicate during interphase to produce two identical sister chromatids.

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.

Anaphase – the chromosomes are divided into single from pair and the chromosomes move to opposite poles

Most telomere are no more that the simple repetition of the DNA nucleotide sequence TTAGGG — two thymine bases, an adenine base, and three guanine bases. With a full length telomere containing more that 15,000 base pairs, telomeres can perform their functions of preventing chromosome from losing coding regions of the genome during replication for many replications before reaching what Dr. Jerry Shay describes as their “critical length” (Shay & Wright). When the telomeres of a cell reach this critical length and can no longer replicate without damaging the base pair sequences of the chromosomes themselves, programmed cell death occurs in the form of apoptosis. However, the length of a chromosome’s telomere is not only a linear function of erosion, but also a function of how often telomerase rebuilds the strands by adding the TTAGGG base pair sequence. It is this way to “cheat” the critical point that provides medicine with the possibility to extend our

The main problem with chromosome instability produced by these breaks is the susceptibility to translocations and thus oncogene activation.

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.

On September 12, 1016, Belmont University graciously allowed Dr. Katherine Friedman from Vanderbilt University to come and talk to a crowd of students about the tendencies of how deoxyribose double stranded breaks can during cell replication and the elements required to hopefully repair this ordeal. She began the session by discussing what chromosomes are composed of and how they are produced, accompanied by visual and statistical representations. Moving on, she touched on how double strand breaks are a huge threat to a cell's, an organisms, stability. Correspondingly, she described what can cause these breaks; chemical factors, as well as inner cell disruptions during replication that are sometimes hard to remedy. However, she also stated that this breaks can occur on purpose, mostly in the immune system in efforts to make antibodies.

What are sister chromosomes and when do they form? How are sister chromatids different from homologous chromosomes?

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.

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

These anti cancer mechanisms depend on p53 and p16ink4 activation, which appear to be responsible for aging similarly to how their failure is associated with cancer. Some other possible mechanisms include heritable mutations and environmental changes in stem cell surroundings. These assumptions are so controversial because adequate models to test the function of these cells have yet to be constructed. Therefore, there I no direct way of determining that stem cell aging is the decrease in stem cell function through regeneration degradation. However, it is an idealistic assumption due to the resulting data of stem cells from other tissues that identify the association between proliferating decline in tissue and aging. A study involving rodents identified that a decline in the quantity of neurons being produced by neural stem cells would decrease with telomere dysfunction. Senescence is a form of growth arrest that is induced by stimuli like loss of telomere function, reactive oxygen species, some DNA damage, and tumor suppressor activation.

Telomere can be described as a weight lifting bar, telomers are at the end of each chromosome like two weights on both ends of a bar. A chromosome is an organelle inside the eukaryotic cell (animal and plant cell), chromosomes obtain genetic information forming genes. Plants, animals, and humans contain trillions of cells throughout their anatomy. How does a telomere relate to genetics? A telomere helps the cell reproduce DNA. Without copying DNA, it is impossible for a cell to live. In 2009 a Noble Prize was won by three experts on heredity discovered the telomere genetic code. One of their significant pieces of this research was in the 1970’s when they did a critical research paper on isolating the sequence of telomeres. They quickly discovered a telomer is used many times each use the telomere breaks off when the DNA is replicated that’s when the length of the telomer shrinks. Before a telomere was discovered Dr. Leonard Hayflick discovered how long a cell can live and his results come out to be 50 to 60 cycles. His results were not understood by scientist but they had faith in his research they quickly understood once the telomer was discovered scientist concluded with a hypothesis if they can control the length of a telomer than I cell can be indestructible it would live forever. Somehow if a discovery came along to uphold a telomer than it could cure cancer, diseases, and provide longer life for a

Telomeres are shortened due to the fact that DNA polymerase are not able to copy the end of the strands that it is replicating. This causes it to shorten, then when it is duplicated once again it is shortened even more, and this process just keeps continuing until the telomere is too short to complete its copying. When telomere lengths become too short, a certain DNA defense goes into action, and this reaction leads to aging. So it is a proven fact that there is a significant relationship between telomere length and the speeding up of physical aging (Prescott, Kraft, & Chasman, 2011).