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In: Biology

What are telomeres, and explain how telomerase prevents the shortening of the linear chromosome. Use illustrations...

  1. What are telomeres, and explain how telomerase prevents the shortening of the linear chromosome. Use illustrations if needed.

Solutions

Expert Solution

Telomere and Telomerase
i.   The replication always takes place from 5′ to 3′ direction in the new strand. The DNA polymerase enzyme is not able to synthesize the new strand at the 5′ end of the new strand. In other words, a small portion (about 300 nucleotides) in the 3′ ends of the parent strands could not be replicated.
ii. This end piece of the chromosome is called telomere. Therefore another enzyme, telomere terminal transferase or telomerase takes up this job of replication of the end piece of chromosomes. The telomeres are noncoding repetitive sequences.
iii. After the normal replication, there is only single strand in this region; so this portion is degraded by exonucleases. This broken end leads to aberrant recombinations or end to end fusions. Unless there is some mechanism to replicate telomeres, the length of the chromosomes will go on reducing at each cell division. The stability of the chromosome is thus lost. Many genes might also be lost in the process.
iv. The shortening of telomere end is prevented by an enzyme telomere terminal transferase or telomerase. It contains an RNA component, which provides the template for telomeric repeat synthesis.
v. Telomerase acts like a reverse transcriptase. Telomerase recognizes 3′ end of telomere, and then a small DNA
strand is synthesized.

Telomerase: This complex contains a protein (Tert) that acts as a reverse transcriptase and a short piece of RNA (Terc) that acts as a template. The CA-rich RNA template base-pairs with the GT-rich, single-stranded 3 -end of telomeric DNA. The reverse transcriptase uses the RNA template to synthesize DNA in the usual 5 →3 direction, extending the already longer 3 -end. Telomerase then translocates to the newly synthesized end, and the process is repeated. Once the GT-rich strand has been lengthened, primase activity of DNA pol α can use it as a template to synthesize an RNA primer. The RNA primer is extended by DNA pol α, and then removed.



vi. Terminal restriction fragments from 70-year old donors are shorter than those from 20-year-old ones. Thus, in old age, the telomerase activity is lost; leading to chromosome instability and cell death.
vii. As a general rule, cancer cells have continued presence of telomerase, and the chromosome length equilibrium is maintained, leading to continued cell division. As cancer cells have increased and persistent activity of telomerase, the cancer cells become immortal. Telomerase is also implicated in other human diseases like diabetes, aplastic anemia, Bloom’s syndrome, Fanconi’s anemia and Ataxia telangiectasia. Elizabeth Blackburn, Carol Greider and Jack Szostak discovered the telomeres and telomerase, all the three were awarded Nobel prize in 2009.
viii. Telomerase is a therapeutic target for cancer chemotherapy. Inhibition of telomerase can effectively control the multiplication of malignant cells. The use of antisense oligonucleotides against the RNA component of the telomerase arrests uncontrolled cell proliferation with minimum side effects.


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