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14.5: DNA Replication in Eukaryotes - Biology

14.5: DNA Replication in Eukaryotes - Biology


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Skills to Develop

  • Discuss the similarities and differences between DNA replication in eukaryotes and prokaryotes
  • State the role of telomerase in DNA replication

Eukaryotic genomes are much more complex and larger in size than prokaryotic genomes. The human genome has three billion base pairs per haploid set of chromosomes, and 6 billion base pairs are replicated during the S phase of the cell cycle. There are multiple origins of replication on the eukaryotic chromosome; humans can have up to 100,000 origins of replication. The rate of replication is approximately 100 nucleotides per second, much slower than prokaryotic replication. In yeast, which is a eukaryote, special sequences known as Autonomously Replicating Sequences (ARS) are found on the chromosomes. These are equivalent to the origin of replication in E. coli.

The number of DNA polymerases in eukaryotes is much more than prokaryotes: 14 are known, of which five are known to have major roles during replication and have been well studied. They are known as pol α, pol β, pol γ, pol δ, and pol ε.

The essential steps of replication are the same as in prokaryotes. Before replication can start, the DNA has to be made available as template. Eukaryotic DNA is bound to basic proteins known as histones to form structures called nucleosomes. The chromatin (the complex between DNA and proteins) may undergo some chemical modifications, so that the DNA may be able to slide off the proteins or be accessible to the enzymes of the DNA replication machinery. At the origin of replication, a pre-replication complex is made with other initiator proteins. Other proteins are then recruited to start the replication process (Table (PageIndex{1})).

A helicase using the energy from ATP hydrolysis opens up the DNA helix. Replication forks are formed at each replication origin as the DNA unwinds. The opening of the double helix causes over-winding, or supercoiling, in the DNA ahead of the replication fork. These are resolved with the action of topoisomerases. Primers are formed by the enzyme primase, and using the primer, DNA pol can start synthesis. While the leading strand is continuously synthesized by the enzyme pol δ, the lagging strand is synthesized by pol ε. A sliding clamp protein known as PCNA (Proliferating Cell Nuclear Antigen) holds the DNA pol in place so that it does not slide off the DNA. RNase H removes the RNA primer, which is then replaced with DNA nucleotides. The Okazaki fragments in the lagging strand are joined together after the replacement of the RNA primers with DNA. The gaps that remain are sealed by DNA ligase, which forms the phosphodiester bond.

Telomere replication

Unlike prokaryotic chromosomes, eukaryotic chromosomes are linear. As you’ve learned, the enzyme DNA pol can add nucleotides only in the 5' to 3' direction. In the leading strand, synthesis continues until the end of the chromosome is reached. On the lagging strand, DNA is synthesized in short stretches, each of which is initiated by a separate primer. When the replication fork reaches the end of the linear chromosome, there is no place for a primer to be made for the DNA fragment to be copied at the end of the chromosome. These ends thus remain unpaired, and over time these ends may get progressively shorter as cells continue to divide.

The ends of the linear chromosomes are known as telomeres, which have repetitive sequences that code for no particular gene. In a way, these telomeres protect the genes from getting deleted as cells continue to divide. In humans, a six base pair sequence, TTAGGG, is repeated 100 to 1000 times. The discovery of the enzyme telomerase (Figure (PageIndex{1})) helped in the understanding of how chromosome ends are maintained. The telomerase enzyme contains a catalytic part and a built-in RNA template. It attaches to the end of the chromosome, and complementary bases to the RNA template are added on the 3' end of the DNA strand. Once the 3' end of the lagging strand template is sufficiently elongated, DNA polymerase can add the nucleotides complementary to the ends of the chromosomes. Thus, the ends of the chromosomes are replicated.

Telomerase is typically active in germ cells and adult stem cells. It is not active in adult somatic cells. For her discovery of telomerase and its action, Elizabeth Blackburn (FIgure (PageIndex{2})) received the Nobel Prize for Medicine and Physiology in 2009.

Telomerase and Aging

Cells that undergo cell division continue to have their telomeres shortened because most somatic cells do not make telomerase. This essentially means that telomere shortening is associated with aging. With the advent of modern medicine, preventative health care, and healthier lifestyles, the human life span has increased, and there is an increasing demand for people to look younger and have a better quality of life as they grow older.

In 2010, scientists found that telomerase can reverse some age-related conditions in mice. This may have potential in regenerative medicine.1 Telomerase-deficient mice were used in these studies; these mice have tissue atrophy, stem cell depletion, organ system failure, and impaired tissue injury responses. Telomerase reactivation in these mice caused extension of telomeres, reduced DNA damage, reversed neurodegeneration, and improved the function of the testes, spleen, and intestines. Thus, telomere reactivation may have potential for treating age-related diseases in humans.

Cancer is characterized by uncontrolled cell division of abnormal cells. The cells accumulate mutations, proliferate uncontrollably, and can migrate to different parts of the body through a process called metastasis. Scientists have observed that cancerous cells have considerably shortened telomeres and that telomerase is active in these cells. Interestingly, only after the telomeres were shortened in the cancer cells did the telomerase become active. If the action of telomerase in these cells can be inhibited by drugs during cancer therapy, then the cancerous cells could potentially be stopped from further division.

Table (PageIndex{1}): Difference between Prokaryotic and Eukaryotic Replication
PropertyProkaryotesEukaryotes
Origin of replicationSingleMultiple
Rate of replication1000 nucleotides/s50 to 100 nucleotides/s
DNA polymerase types514
TelomeraseNot presentPresent
RNA primer removalDNA pol IRNase H
Strand elongationDNA pol IIIPol δ, pol ε
Sliding clampSliding clampPCNA

Summary

Replication in eukaryotes starts at multiple origins of replication. The mechanism is quite similar to prokaryotes. A primer is required to initiate synthesis, which is then extended by DNA polymerase as it adds nucleotides one by one to the growing chain. The leading strand is synthesized continuously, whereas the lagging strand is synthesized in short stretches called Okazaki fragments. The RNA primers are replaced with DNA nucleotides; the DNA remains one continuous strand by linking the DNA fragments with DNA ligase. The ends of the chromosomes pose a problem as polymerase is unable to extend them without a primer. Telomerase, an enzyme with an inbuilt RNA template, extends the ends by copying the RNA template and extending one end of the chromosome. DNA polymerase can then extend the DNA using the primer. In this way, the ends of the chromosomes are protected.

  1. 1 Jaskelioff et al., “Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice,” Nature 469 (2011): 102-7.

Glossary

telomerase
enzyme that contains a catalytic part and an inbuilt RNA template; it functions to maintain telomeres at chromosome ends
telomere
DNA at the end of linear chromosomes

DNA Replication in Eukaryotes | Genetics

In this article we will discuss about the DNA replication in eukaryotes.

In eukaryotes there are only two different types of DNA polymerases in contrast with DNA polymerase I, II and III of prokaryotes. Furthermore the DNA of eukaryotes is a long linear molecule with several replication units. A diploid mammalian cell contains on an average about 6 pg of DNA in the G phase. This much DNA is equivalent to a length of 2 metres of a linear DNA molecule.

If a single replication unit were to move along this length of DNA, it could complete replication within the 8 hour S phase only if its rate of movement is about 4 mm/min. This is obviously a very fast rate.

The replicating fork actually moves at a slower speed (0.5 to 2.0 micron/min.) in eukaryotes adding about 2,600 bases per minute. In E. coli it moves faster adding about 6,000 bases per minute. It is, therefore, necessary that in eukaryotes replication be initiated at several points of origin.

Auto-radiographic studies on labelling patterns of individual metaphase chromosomes have shown that multiple adjacent units initiate replication simultaneously. The most convincing demonstration however, came from similar observations in giant polytene chromosomes.

Here tritiated thymidine is incorporated simultaneously into a large number of different bands. By the same technique the egg in Drosophila is shown to have 6,000 replication forks and all the DNA synthesis is completed within 3 minutes.

The unit of replication is the replicon. The size of the replicon is estimated from the distance between adjacent initiation points (centre-to-centre distance). By autoradiography it has been found that units within the same cell are not uniform in size but fall within the range of 15-60 micron.

Replicons in rapidly growing cells with short S phases are smaller than those in cells growing more slowly with longer S phases. Blumenthal (1973) has estimated that in Drosophila melanogaster replicons in embryonic cells are as short as 3-4 micron, whereas in a cell line of the same species they were about 13 micron long.

Experimental studies on cultured mammalian (Chinese hamster) cells have shown that the rate of DNA synthesis is not constant throughout the S phase, Kleveroz (1975) found that synthesis is slow at the beginning of S phase, thereafter it increases. About 50% of replication occurs during the last hour of the 5.5 hour long S phase.

The occurrence of multiple adjacent units has led to the concept that replication units exist in clusters. All units in a cluster do not replicate simultaneously, some being late replicating. In mammalian cells there are about 100 replicating units in a cluster.

The essential features of DNA replication are similar in eukaryotes and prokaryotes. After replication begins at a central point of origin in each unit, it proceeds in both directions away from the initiation site. Chain growth occurs by means of fork-like growing points. Electron micrographs therefore show a number of ‘eyes’ or ‘bubbles’, each formed between two replicating forks along the linear molecule.

It appears that there are no specific term in DNA for stopping replication. The forks travel towards each other and the newly synthesised chains meet and fuse with chains synthesised on adjacent units (Fig. 14.11). In this way long DNA duplexes characteristic of eukaryotic chromosomes are produced.

As in prokaryotes, the first step in DNA synthesis in eukaryotes is the formation of a primer strand of RNA about 10 nucleotides in length—catalysed by the enzyme RNA polymerase. After that DNA polymerase takes over and adds deoxyribonucleotides to the 3′ end of the primer RNA.

The Okazaki fragments thus formed are shorter in eukaryotes (about 100-150 nucleotides long) than in prokaryotes (1,000 to 2,000 nucleotides). The gaps between the fragments are filled up against the parent DNA template and their ends are joined by DNA ligase enzyme. The RNA primer is digested, starting from its 5′ end by the exonuclease activity of DNA polymerase.

Significance of the RNA Primer in DNA Synthesis:

Why should DNA replication be initiated by the enzyme RNA polymerase and formation of RNA strand take place? Detailed analysis of DNA polymerase enzymes have revealed the fact that each polymerase enzyme can add nucleotides only to an already existing polynucleotide chain.

These enzymes are not able to initiate new DNA chains. The point of origin in a DNA duplex is perhaps recognised by RNA polymerase, the enzyme which catalyses the synthesis of RNA on a DNA template. In other words, RNA polymerase is required for both RNA and DNA synthesis.

Synthesis of RNA primer on the DNA template continues until a stop signal is reached. The enzyme is then released and the RNA chain serves as a primer for addition of DNA nucleotides by DNA polymerase enzyme. However, the molecular mechanism which initiates DNA replication is not fully known.


A protein complex called the Origin Recognition Complex (ORC) binds at the origin of replication sequence in the DNA during late M phase/G1 phase of the cell cycle. The ORC interacts with a few other proteins, one known as Cdc6 works with another protein called Cdt1 to help load a complex of proteins known as helicase onto the DNA. (Remember that DNA helicases use ATP to unwind the DNA helix by breaking the hydrogen bonds between paired bases.) The ORC/Cdc6/Cdt1/Helicase complex along with other associated proteins is known as the pre-replicative complex or pre-RC (Figure 14-1). The pre-RC persists until the G1/S transition, which occurs once the cell receives a signal to divide. At the G1/S transition, it is thought that Cdc6 and Cdt1 unbind from the pre-RC and other proteins that are responsible for recruiting additional DNA replication proteins associate with the helicase to form the pre-initiation complex. Interestingly, the ORC is inhibitory to replication and must be removed before replication can proceed.

Figure 14-1: Licensing of Replication. In late M phase/early G1, origin recognition (ORC) proteins recognize the origin of replication (Ori), shown in green. These recruit many proteins, one is Cdc6, which helps recruit helicase. This establishes the pre-initiation replication complex (Pre-RC). Activation of replication occurs during early S phase, once the ORC, Cdc6, the helicase and several other proteins (not shown) are phosphorylated by the S-phase CDK/cyclin. Phosphorylation of ORC and Cdc6 cause the proteins to be deactivated, while phosphorylation of the helicase causes the protein to be activated. (Attributed to Devin A. King)

At this point, the activated S-phase CDK/cyclin phosphorylates several proteins to start or ‘fire’ replication. One of the proteins the S-phase CDK/cyclin phosphorylates is Cdc6, which helps target this protein for degradation. Additionally, the ORC is phosphorylated to prevent it from being used a second time (or rebinding the origin of replication) and phosphorylation is thought reduce the binding affinity of ORC for the origin. The helicase is also phosphorylated to activate it and encourage it to begin unwinding the DNA. Thus, these three phosphorylation events, and many others not described here, help facilitate the start of DNA replication.

The opening of the double helix by helicase causes over-winding, or supercoiling, in the DNA ahead of the replication fork. These are resolved by the action of topoisomerases , which cut the phosphodiester backbone to release torsional strain and then re-ligate the strand back together. Additionally, opening the helix makes the DNA single-stranded. To prevent the DNA strands from reannealing before being replicated and to protect them from chemical modifications from their environment, proteins called single-stranded DNA binding proteins (SSBs) are associated with the DNA.


14.5: DNA Replication in Eukaryotes - Biology

Most prokaryotic factors utilized during replication have equivalents that play similar roles in eukaryotic DNA duplication.

This process initiates at an origin of replication, to which a recognition complex binds. Helicase is then attracted to the site and separates the strands of DNA, generating a bubble with two forks.

Primase also arrives and generates RNA primers, which, as helicase moves, DNA polymerase elongates with new DNA. As in prokaryotes, the newly-formed leading strand grows continuously, following the replication fork.

Conversely, the lagging strand is manufactured in small Okazaki fragments, traveling opposite the fork.

Due to multiple factors, the DNA template used to generate the leading strand in 1/2 of this structure creates the lagging strand in the other.

Interestingly, various origins of replication exist on a linear eukaryotic chromosome, and replication terminates when their associated spheres coalesce. Primers are then eliminated via enzymes like RNAse and swapped for DNA. Afterwards, DNA ligase attaches any segments.

However, when the end primer disappears from the lagging strand, the space remains empty, and there is an uncopied stretch of DNA template abutting it. To combat this, an enzyme called telomerase affixes to the overhanging region and elongates it with a non-coding DNA sequence.

Primase and DNA polymerase act upon this extended region, creating a telomere cap that protects against loss of coding DNA from the lagging strand during multiple replications.

Thus eukaryotic DNA replication ends with two DNA molecules, each with a parental and newly-synthesized strand, numerous origins of replication, and telomeres.

13.6: Replication in Eukaryotes

Overview

In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.

Many Proteins Orchestrate Replication at the Origin

Eukaryotic replication follows many of the same principles as prokaryotic DNA replication, but because the genome is much larger and the chromosomes are linear rather than circular, the process requires more proteins and has a few key differences. Replication occurs simultaneously at multiple origins of replication along each chromosome. Initiator proteins recognize and bind to the origin, recruiting helicase to unwind the DNA double helix. At each point of origin, two replication forks form. Primase then adds short RNA primers to the single strands of DNA, which serve as a starting point for DNA polymerase to bind and begin copying the sequence. DNA can only be synthesized in the 5&rsquo to 3&rsquo direction, so replication of both strands from a single replication fork proceeds in two different directions. The leading strand is synthesized continuously, while the lagging strand is synthesized in short stretches 100-200 base pairs in length, called Okazaki fragments. Once the bulk of replication is complete, RNase enzymes remove the RNA primers and DNA ligase joins any gaps in the new strand.

Dividing the Work of Replication among Polymerases

The workload of copying DNA in eukaryotes is divided among multiple different types of DNA polymerase enzymes. Major families of DNA polymerases across all organisms are categorized by the similarity of their protein structures and amino acid sequences. The first families to be discovered were termed A, B, C, and X, with families Y and D identified later. Family B polymerases in eukaryotes include Pol &alpha, which also functions as a primase at the replication fork, and Pol &delta and &epsilon, the enzymes that do most of the work of DNA replication on the leading and lagging strands of the template, respectively. Other DNA polymerases are responsible for such tasks as repairing DNA damage,copying mitochondrial and plastid DNA, and filling in gaps in the DNA sequence on the lagging strand after the RNA primers are removed.

Telomeres Protect the Ends of the Chromosomes from Degradation

Because eukaryotic chromosomes are linear, they are susceptible to degradation at the ends. To protect important genetic information from damage, the ends of chromosomes contain many non-coding repeats of highly conserved G-rich DNA: the telomeres. A short single-stranded 3&rsquo overhang at each end of the chromosome interacts with specialized proteins, which stabilizes the chromosome within the nucleus. Because of the manner in which the lagging strand is synthesized, a small amount of the telomeric DNA cannot be replicated with each cell division. As a result, the telomeres gradually get shorter over the course of many cell cycles and they can be measured as a marker of cellular aging. Certain populations of cells, such as germ cells and stem cells, express telomerase, an enzyme that lengthens the telomeres, allowing the cell to undergo more cell cycles before the telomeres shorten.

Garcia-Diaz, Miguel, and Katarzyna Bebenek. &ldquoMultiple functions of DNA polymerases.&rdquo Critical Reviews in Plant Sciences 26 (2007): 105-122. [Source]


Telomere replication

Unlike prokaryotic chromosomes, eukaryotic chromosomes are linear. As you&rsquove learned, the enzyme DNA pol can add nucleotides only in the 5' to 3' direction. In the leading strand, synthesis continues until the end of the chromosome is reached. On the lagging strand, DNA is synthesized in short stretches, each of which is initiated by a separate primer. When the replication fork reaches the end of the linear chromosome, there is no place for a primer to be made for the DNA fragment to be copied at the end of the chromosome. These ends thus remain unpaired, and over time these ends may get progressively shorter as cells continue to divide.


Telomerase and Aging

Cells that undergo cell division continue to have their telomeres shortened because most somatic cells do not make telomerase. This essentially means that telomere shortening is associated with aging. With the advent of modern medicine, preventative health care, and healthier lifestyles, the human life span has increased, and there is an increasing demand for people to look younger and have a better quality of life as they grow older.

In 2010, scientists found that telomerase can reverse some age-related conditions in mice. This may have potential in regenerative medicine. 1 Telomerase-deficient mice were used in these studies these mice have tissue atrophy, stem cell depletion, organ system failure, and impaired tissue injury responses. Telomerase reactivation in these mice caused extension of telomeres, reduced DNA damage, reversed neurodegeneration, and improved the function of the testes, spleen, and intestines. Thus, telomere reactivation may have potential for treating age-related diseases in humans.

Cancer is characterized by uncontrolled cell division of abnormal cells. The cells accumulate mutations, proliferate uncontrollably, and can migrate to different parts of the body through a process called metastasis. Scientists have observed that cancerous cells have considerably shortened telomeres and that telomerase is active in these cells. Interestingly, only after the telomeres were shortened in the cancer cells did the telomerase become active. If the action of telomerase in these cells can be inhibited by drugs during cancer therapy, then the cancerous cells could potentially be stopped from further division.

Difference between Prokaryotic and Eukaryotic Replication
Property Prokaryotes Eukaryotes
Origin of replication Single Multiple
Rate of replication 1000 nucleotides/s 50 to 100 nucleotides/s
DNA polymerase types 5 14
Telomerase Not present Present
RNA primer removal DNA pol I RNase H
Strand elongation DNA pol III Pol δ, pol ε
Sliding clamp Sliding clamp PCNA


Telomerase and Aging

Cells that undergo cell division continue to have their telomeres shortened because most somatic cells do not make telomerase. This essentially means that telomere shortening is associated with aging. With the advent of modern medicine, preventative health care, and healthier lifestyles, the human life span has increased, and there is an increasing demand for people to look younger and have a better quality of life as they grow older.

In 2010, scientists found that telomerase can reverse some age-related conditions in mice. This may have potential in regenerative medicine. Jaskelioff et al., “Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice,” Nature 469 (2011): 102-7. Telomerase-deficient mice were used in these studies these mice have tissue atrophy, stem cell depletion, organ system failure, and impaired tissue injury responses. Telomerase reactivation in these mice caused extension of telomeres, reduced DNA damage, reversed neurodegeneration, and improved the function of the testes, spleen, and intestines. Thus, telomere reactivation may have potential for treating age-related diseases in humans.

Cancer is characterized by uncontrolled cell division of abnormal cells. The cells accumulate mutations, proliferate uncontrollably, and can migrate to different parts of the body through a process called metastasis. Scientists have observed that cancerous cells have considerably shortened telomeres and that telomerase is active in these cells. Interestingly, only after the telomeres were shortened in the cancer cells did the telomerase become active. If the action of telomerase in these cells can be inhibited by drugs during cancer therapy, then the cancerous cells could potentially be stopped from further division.

Difference between Prokaryotic and Eukaryotic Replication
PropertyProkaryotesEukaryotes
Origin of replicationSingleMultiple
Rate of replication1000 nucleotides/s50 to 100 nucleotides/s
DNA polymerase types514
TelomeraseNot presentPresent
RNA primer removalDNA pol IRNase H
Strand elongationDNA pol IIIPol δ, pol ε
Sliding clampSliding clampPCNA


What is Eukaryotic DNA Replication?

The replication events at the replication fork arc much the same in eukaryotes as in prokaryotes except that the enzymes and protein factors are different. The main polymerizing enzyme is polymerase a, (3, y, 8 & e.

This polymerase enzyme is much slower in comparison to that of prokaiyote. DNA pol III adds about 1000 nucleotides per second where as DXA pol a ads about 50 nucleotides per second. The SSB protein is known as Replication factor A in eukaryote and the topoisomerase is Type I topoisomerase.

Another big difference is the sheer amount of DXA and the larger size of DXA. Eukaryotes have more than one chromosomes and cach chromosome has DXA larger than the genome of a bacterium. For example, the total length of human DXA of one cell is about 2 meter where as that of E.coli is only l mm. So for larger DXA to replicate in quick time eukaryotic DXA have multiple origin and cach eukaryotic DXA is a multiple replicon.

The yeast cell chromosomes have about 400 origin and cach human DXA with about 1000 origins. Imagine a situation of human genome with 4xio 9 base pairs to rcplicate as a single replieon: it will take several weeks. But, the cell cyclc is completed in 24 hours and for that cycle to operate in time, the DXA replication in human is completed in 6-8 hours of S-phase. This is achieved due to the presence of multiple origins.

During the S-phase of the cell cycle, the DXA replicates only once and then the cell divides. Hence the amount of total DXA is first doubled in S-phase and then equally divided between the two daughter cells during the cell division. Thus the DXA level (and the chromosome number) is kept constant after successive cell divisions.

The accurate replication of DXA and their equal distribution among the daughter cells form the bases of transmission of hereditary characters. Any error in DXA replication is taken care of by DXA repair mechanism available in the cell. But, imagine a situation where DXA divides not once but many times before a cell division. In such a situation the total DXA will increase two times, four times or many more times and the subsequent cell division will produce polyploid cells (cells with more than the normal number of chromosomes).

This does not happen as the cells have a replication licensing system. During the cell division, in the anaphase stage the replication origins are licensed by a nondiffusible Replication Licensing Factors or RLF. After the anaphase, no further licensing can occur due to the presence of nuclear membrane.

The RLF allows DNA to replicate once in the S-phase and the RLF get destroyed during replication. Further round of replication will require further licensing. Unless the cell undertakes division cycle, it cannot come to anaphase and licensing of origins cannot occur. This mechanism ensures that a cell must divide after a single round of DNA replication.


Telomere replication

Unlike prokaryotic chromosomes, eukaryotic chromosomes are linear. As you’ve learned, the enzyme DNA pol can add nucleotides only in the 5' to 3' direction. In the leading strand, synthesis continues until the end of the chromosome is reached. On the lagging strand, DNA is synthesized in short stretches, each of which is initiated by a separate primer. When the replication fork reaches the end of the linear chromosome, there is no place for a primer to be made for the DNA fragment to be copied at the end of the chromosome. These ends thus remain unpaired, and over time these ends may get progressively shorter as cells continue to divide.

The ends of the linear chromosomes are known as telomeres, which have repetitive sequences that code for no particular gene. In a way, these telomeres protect the genes from getting deleted as cells continue to divide. In humans, a six base pair sequence, TTAGGG, is repeated 100 to 1000 times. The discovery of the enzyme telomerase (Figure) helped in the understanding of how chromosome ends are maintained. The telomerase enzyme contains a catalytic part and a built-in RNA template. It attaches to the end of the chromosome, and complementary bases to the RNA template are added on the 3' end of the DNA strand. Once the 3' end of the lagging strand template is sufficiently elongated, DNA polymerase can add the nucleotides complementary to the ends of the chromosomes. Thus, the ends of the chromosomes are replicated.

The ends of linear chromosomes are maintained by the action of the telomerase enzyme.

Telomerase is typically active in germ cells and adult stem cells. It is not active in adult somatic cells. For her discovery of telomerase and its action, Elizabeth Blackburn (Figure) received the Nobel Prize for Medicine and Physiology in 2009.

Elizabeth Blackburn, 2009 Nobel Laureate, is the scientist who discovered how telomerase works. (credit: US Embassy Sweden)


Summary – Prokaryotic vs Eukaryotic Transcription

Transcription is the first step of gene expression, which is followed by translation. Though the transcription mechanism is the same in prokaryotes and eukaryotes, there are several differences between them. The key difference between prokaryotic and eukaryotic transcription is that the prokaryotic transcription occurs in the cytoplasm while the eukaryotic transcription occurs in the nucleus. Furthermore, prokaryotic transcription involves only one RNA polymerase while eukaryotic transcription involves three types of RNA polymerases. Moreover, the mRNA sequence of prokaryotes is polycistronic while in eukaryotes, mRNA sequence is monocistronic. Not only that, in eukaryotes, post-transcriptional modifications occur while in prokaryotes, they do not occur. This is the summary of the difference between prokaryotic and eukaryotic transcription.

Reference:

1. Cooper, Geoffrey M. “Transcription in Prokaryotes.” Current Neurology and Neuroscience Reports., U.S. National Library of Medicine, 1 Jan. 1970. Available here
2. “Eukaryotic Transcription.” Wikipedia, Wikimedia Foundation, 17 Jan. 2019. Available here

Image Courtesy:

1.”Bacterial Protein synthesis”By Joan L. Slonczewski, John W. Foster – Microbiology: An Evolving Science, (CC BY-SA 3.0) via Commons Wikimedia
2.”Eukaryotic Transcription”By Frank Starmer (CC BY 1.0) via Commons Wikimedia


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