TELOMERES AND CENTROMERES:Definition and Function

0 0
Read Time:3 Minute, 54 Second

TELOMERES AND CENTROMERES Simplified

TELOMERE

“TELOMERES AND CENTROMERES” A telomere is a region of repetitive nucleotide sequences at each end of a chromosome, which protects the end of the chromosome from deterioration or from fusion with neighbouring chromosomes.

DNA replication cannot extend all the way to the end of a chromosome. This will result in losing sequences and information with each round of replication. The solution for our cells is a simple repeating unit (TTAGGG) at the end of the DNA, forming a telomere. Some of the sequences are lost in each round of replication and can be replaced by the enzyme telomerase.

Telomeres are like Lids at the end of each strand of DNA that protects chromosomes. without telomeres, DNA strands become damaged and cells can’t do their job. Animal studies indicate that there are a set number of replications possible and that the progressive shortening of telomeres contributes to ageing.

telomere

Centromere “TELOMERES AND CENTROMERES”

 

The centromere is a very specific part of the chromosome. It is found not always right in the middle, but somewhere between one-third and two-thirds of the way down the chromosome. It is the part where the cell’s chromosomes are constricted, they are often referred to as sites of constriction because they form noticeable indentations. They are composed of heterochromatin, which is in turn composed of tandem repeat sequences that contain high GC-content. They’re a little bit tighter and almost looks like a little ball in the middle of two sticks. The centromere is what separates the chromosome into what is called, for human chromosomes, the P and Q arm. And these P and Q arms are a part of is used in cytogenetics to determine many chromosomes are present in a cell and what chromosome number they are.

centromere

REPLICATING THE ENDS OF CHROMOSOMES
While DNA polymerase does an excellent job of synthesizing DNA, it, unfortunately, cannot complete synthesis of the 5′ end of the strand. Thus, each time DNA synthesis is carried out, the chromosome becomes a little shorter. To lengthen the time that cells can replicate and synthesize DNA before necessary genes are damaged, chromosomes contain telomeres. As described earlier, telomeres are located at the very tips of the chromosome and consist of repetitive sequences with a high GC content. This repetition means that telomeres can be slightly degraded between replication cycles without loss of function.

 

DNA REPAIR
The structure of DNA can be damaged in a number of ways such as exposure to chemicals or radiation. DNA is very susceptible to damage and if the damage is not corrected, it will subsequently be copied and passed on to daughter cells. Damage can include breaking of the DNA backbone, structural or spontaneous alterations of bases or incorporation of the incorrect base during replication. Any defect in the genetic code can cause an increased risk of cancer, so the cell has multiple processes in place to catch and correct genetic errors. This helps maintain the integrity and stability of the genome from cell to cell, and from generation to generation.

ONCOGENES AND TUMOR SUPPRESSOR GENES
Certain genes, when mutated, can lead to cancer. Cancer cells proliferate excessively because they are able to divide without stimulation from other cells and are no longer subject to the normal controls on cell proliferation. By definition, cancer cells are able to migrate by local invasion or metastasis, a migration to distant tissues by the bloodstream or lymphatic system. Over time, cancer cells tend to accumulate mutations. Mutated genes that cause cancer are termed oncogenes. Oncogenes primarily encode cell cycle-related proteins. Before these genes are mutated, they are often referred to as proto-oncogenes. The first gene in this category to be discovered was src (named after sarcoma, a category of connective tissue cancers). The abnormal alleles encode proteins that are more active than normal proteins, promoting rapid cell cycle advancement. Typically, a mutation in only one copy is sufficient to promote tumour growth and is therefore considered dominant. Tumour suppressor genes, like p53 or Rb (retinoblastoma), encode proteins that inhibit the cell cycle or participate in DNA repair processes. They normally function to stop tumour progression and are sometimes called antioncogenes. Mutations of these genes result in the loss of tumour suppression activity and therefore promote cancer. Inactivation of both alleles is necessary for the loss of function because, in most cases, even one copy of the normal protein can function to inhibit tumour formation. In this example, multiple mutations or hits are required.

I would love to hear your thoughts

Happy
Happy
0 %
Sad
Sad
0 %
Excited
Excited
0 %
Sleepy
Sleepy
0 %
Angry
Angry
0 %
Surprise
Surprise
0 %

Related Posts

Average Rating

5 Star
0%
4 Star
0%
3 Star
0%
2 Star
0%
1 Star
0%

Leave a Reply

Your email address will not be published.