why would cells ever apply non-homologous end joining if there is a cleaner and safer alternative? Do they only do that when there's no undamaged template available?

In the absense of homologous chromosome (when DNA hasn't undegone replication yet) non homologous end joining is done.

Is there potential, during any of the above proofreading methods to "correct" the template DNA rather than the newly-formed strand?

By potential, do you mean that is mistakenly correcting the template strand possible? If so, then yes it is. The mechanism to determine which is the newly-formed and the template strand isn't perfect and relies on methylation and other epigenetic markers. These can fail. If the damage includes these markers, or the damage/defective piece is extensive so as to avoid these markers from being introduced, or if the damage doesn't allow the DNA repair machinery to sense these markers, it is very much possible the correction is faulty. Some repair machineries are anyway strand non-specific, and some are even sequence non-specific (see Non Homologous End Joining, which is the last resort at DNA stability).

Why is thymine in DNA and uracil in RNA?

Thymine is the nucleotide that DNA uses. RNA is not the same thing as DNA so it seems very natural that the two of them would have some differences. Uracil is one of them.

what happen if DNA have uracil instead of uracil ? how can DNA repair it ? and what are the reasons that DNA contain thymine not uracil

In your question – "what happen if DNA have uracil instead of uracil ?" — I am assuming your second "uracil" was supposed to be "thymine" ... I'm not sure what you really want to know — as it says in the article, uracil in DNA is usually recognized as a mistake and removed by the `Base Excision Repair` pathway ... There are a number of proposed reasons why thymine is used in DNA. 1) Cytosine residues in DNA undergo a spontaneous change that converts them into uracil. There are enzymes that specifically recognize and remove uracil (but not thymine) from DNA and this helps suppress what would otherwise be a major contributor to the rate mutations. 2) Thymine is chemically more stable (though slightly more expensive to make), so this again probably helps reduce the mutation rate. An interesting and detailed discussion of these factors and more can be found here: http://www.scienceinschool.org/2011/issue18/uracil If you have further questions please leave a comment.

In the Mismatch repair, why is a section of DNA cut off rather than only the mismatched base pair cut off?

So it depends on the mechanism used. Base excision repair only removes one base (deaminated cytosine for example). Nucleotide excision repair is used with thymine dimers when the DNA is warped, and in that case it removes a 12-24 nucleotide section. Generally proteins are not very wasteful.

What occurs in cancerous cells when going through mismatch repair? Is the issue ignored? Or is it because the cancerous cell had gone through mismatch repair, then became cancerous?

In cancer cells, the mismatch repair has not happened. This leads to mutations. This is a classic example: https://en.wikipedia.org/wiki/Xeroderma_pigmentosum Without the nucleotide excision repair system, the individual develops melanoma and/or carcinoma at a very young age. Also recall that skin cancer metastasizes to the lungs, so this is a very bad prognosis indeed.

How the proteins involved in DNA repair detect the fault?

It depends on what is wrong. For example, some damage distorts the shape of the DNA helix, and there are proteins scanning the genome for this. Sometimes damage is detected when an RNA polymerase stalls. In mismatch repair, there are proteins involved that detect the mismatch, and proteins that detect which is the old and which is the newly synthesised DNA strand.

Why is thymine in DNA and uracil in RNA?

Uracil is the cheapest to produce energetically, and is therefore favored at the RNA level where fidelity is not as important and large quantities are produced.

Main content

Course: Biology library > Unit 17

Lesson 3: DNA replication

DNA proofreading and repair

Google Classroom

Mechanisms to correct errors during DNA replication and to repair DNA damage over the cell's lifetime.

Key points:

Cells have a variety of mechanisms to prevent mutations, or permanent changes in DNA sequence.
During DNA synthesis, most DNA polymerases "check their work," fixing the majority of mispaired bases in a process called proofreading.
Immediately after DNA synthesis, any remaining mispaired bases can be detected and replaced in a process called mismatch repair.
If DNA gets damaged, it can be repaired by various mechanisms, including chemical reversal, excision repair, and double-stranded break repair.

Introduction

What does DNA have to do with cancer? Cancer occurs when cells divide in an uncontrolled way, ignoring normal "stop" signals and producing a tumor. This bad behavior is caused by accumulated mutations, or permanent sequence changes in the cells' DNA.

Replication errors and DNA damage are actually happening in the cells of our bodies all the time. In most cases, however, they don’t cause cancer, or even mutations. That’s because they are usually detected and fixed by DNA proofreading and repair mechanisms. Or, if the damage cannot be fixed, the cell will undergo programmed cell death (apoptosis) to avoid passing on the faulty DNA.

Mutations happen, and get passed on to daughter cells, only when these mechanisms fail. Cancer, in turn, develops only when multiple mutations in division-related genes accumulate in the same cell.

In this article, we’ll take a closer look at the mechanisms used by cells to correct replication errors and fix DNA damage, including:

Proofreading, which corrects errors during DNA replication
Mismatch repair, which fixes mispaired bases right after DNA replication
DNA damage repair pathways, which detect and correct damage throughout the cell cycle

Proofreading

DNA polymerases are the enzymes that build DNA in cells. During DNA replication (copying), most DNA polymerases can “check their work” with each base that they add. This process is called proofreading. If the polymerase detects that a wrong (incorrectly paired) nucleotide has been added, it will remove and replace the nucleotide right away, before continuing with DNA synthesis

^{1}

Mismatch repair

Many errors are corrected by proofreading, but a few slip through. Mismatch repair happens right after new DNA has been made, and its job is to remove and replace mis-paired bases (ones that were not fixed during proofreading). Mismatch repair can also detect and correct small insertions and deletions that happen when the polymerases "slips," losing its footing on the template

^{2}

How does mismatch repair work? First, a protein complex (group of proteins) recognizes and binds to the mispaired base. A second complex cuts the DNA near the mismatch, and more enzymes chop out the incorrect nucleotide and a surrounding patch of DNA. A DNA polymerase then replaces the missing section with correct nucleotides, and an enzyme called a DNA ligase seals the gap

^{2}

One thing you may wonder is how the proteins involved in DNA repair can tell "who's right" during mismatch repair. That is, when two bases are mispaired (like the G and T in the drawing above), which of the two should be removed and replaced?

In bacteria, original and newly made strands of DNA can be told apart by a feature called methylation state. An old DNA strand will have methyl (

- {CH}_{3}

) groups attached to some of its bases, while a newly made DNA strand will not yet have gotten its methyl group

^{3}

In eukaryotes, the processes that allow the original strand to be identified in mismatch repair involve recognition of nicks (single-stranded breaks) that are found only in the newly synthesized DNA

^{3}

DNA damage repair mechanisms

Bad things can happen to DNA at almost any point in a cell's lifetime, not just during replication. In fact, your DNA is getting damaged all the time by outside factors like UV light, chemicals, and X-rays—not to mention spontaneous chemical reactions that happen even without environmental insults!

^{4}

Fortunately, your cells have repair mechanisms to detect and correct many types of DNA damage. Repair processes that help fix damaged DNA include:

Direct reversal: Some DNA-damaging chemical reactions can be directly "undone" by enzymes in the cell.
Excision repair: Damage to one or a few bases of DNA is often fixed by removal (excision) and replacement of the damaged region. In base excision repair, just the damaged base is removed. In nucleotide excision repair, as in the mismatch repair we saw above, a patch of nucleotides is removed.
Double-stranded break repair: Two major pathways, non-homologous end joining and homologous recombination, are used to repair double-stranded breaks in DNA (that is, when an entire chromosome splits into two pieces).

Reversal of damage

In some cases, a cell can fix DNA damage simply by reversing the chemical reaction that caused it. To understand this, we need to realize that "DNA damage" often just involves an extra group of atoms getting attached to DNA through a chemical reaction.

For example, guanine (G) can undergo a reaction that attaches a methyl (

- {CH}_{3}

) group to an oxygen atom in the base. The methyl-bearing guanine, if not fixed, will pair with thymine (T) rather than cytosine (C) during DNA replication. Luckily, humans and many other organisms have an enzyme that can remove the methyl group, reversing the reaction and returning the base to normal

^{5}

Base excision repair

Base excision repair is a mechanism used to detect and remove certain types of damaged bases. A group of enzymes called glycosylases play a key role in base excision repair. Each glycosylase detects and removes a specific kind of damaged base.

For example, a chemical reaction called deamination can convert a cytosine base into uracil, a base typically found only in RNA. During DNA replication, uracil will pair with adenine rather than guanine (as it would if the base was still cytosine), so an uncorrected cytosine-to-uracil change can lead to a mutation

^{5}

To prevent such mutations, a glycosylase from the base excision repair pathway detects and removes deaminated cytosines. Once the base has been removed, the "empty" piece of DNA backbone is also removed, and the gap is filled and sealed by other enzymes

^{6}

Nucleotide excision repair

Nucleotide excision repair is another pathway used to remove and replace damaged bases. Nucleotide excision repair detects and corrects types of damage that distort the DNA double helix. For instance, this pathway detects bases that have been modified with bulky chemical groups, like the ones that get attached to your DNA when it's exposed to chemicals in cigarette smoke

^{7}

Nucleotide excision repair is also used to fix some types of damage caused by UV radiation, for instance, when you get a sunburn. UV radiation can make cytosine and thymine bases react with neighboring bases that are also Cs or Ts, forming bonds that distort the double helix and cause errors in DNA replication. The most common type of linkage, a thymine dimer, consists of two thymine bases that react with each other and become chemically linked

^{8}

In nucleotide excision repair, the damaged nucleotide(s) are removed along with a surrounding patch of DNA. In this process, a helicase (DNA-opening enzyme) cranks open the DNA to form a bubble, and DNA-cutting enzymes chop out the damaged part of the bubble. A DNA polymerase replaces the missing DNA, and a DNA ligase seals the gap in the backbone of the strand

^{9}

Double-stranded break repair

Some types of environmental factors, such as high-energy radiation, can cause double-stranded breaks in DNA (splitting a chromosome in two). This is the kind of DNA damage linked with superhero origin stories in comic books, and with disasters like Chernobyl in real life.

Double-stranded breaks are dangerous because large segments of chromosomes, and the hundreds of genes they contain, may be lost if the break is not repaired. Two pathways involved in the repair of double-stranded DNA breaks are the non-homologous end joining and homologous recombination pathways.

In non-homologous end joining, the two broken ends of the chromosome are simply glued back together. This repair mechanism is “messy” and typically involves the loss, or sometimes addition, of a few nucleotides at the cut site. So, non-homologous end joining tends to produce a mutation, but this is better than the alternative (loss of an entire chromosome arm)

^{10}

In homologous recombination, information from the homologous chromosome that matches the damaged one (or from a sister chromatid, if the DNA has been copied) is used to repair the break. In this process, the two homologous chromosomes come together, and the undamaged region of the homologue or chromatid is used as a template to replace the damaged region of the broken chromosome. Homologous recombination is “cleaner” than non-homologous end joining and does not usually cause mutations

^{11}

DNA proofreading and repair in human disease

Evidence for the importance of proofreading and repair mechanisms comes from human genetic disorders. In many cases, mutations in genes that encode proofreading and repair proteins are associated with heredity cancers (cancers that run in families). For example:

Hereditary nonpolyposis colorectal cancer (also called Lynch syndrome) is caused by mutations in genes encoding certain mismatch repair proteins $^{12, 13}$ ‍. Since mismatched bases are not repaired in the cells of people with this syndrome, mutations accumulate much more rapidly than in the cells of an unaffected person. This can lead to the development of tumors in the colon.
People with xeroderma pigmentosum are extremely sensitive to UV light. This condition is caused by mutations affecting the nucleotide excision repair pathway. When this pathway doesn't work, thymine dimers and other forms of UV damage can't be repaired. People with xeroderma pigmentosum develop severe sunburns from just a few minutes in the sun, and about half will get skin cancer by the age of $10$ ‍ unless they avoid the sun $^{14}$ ‍.

This article is licensed under a CC BY-NC-SA 4.0 license.

Works cited:

Berg, J. M., Tymoczko, J. L., and Stryer, L. (2002). DNA polymerases require a template and primer. In _Biochemistry (5th ed., section 27.2.4). New York, NY: W. H. Freeman, 2002. http://www.ncbi.nlm.nih.gov/books/NBK22374/#_A3777_.
Dexheimer, T. S. (2013). DNA repair pathways and mechanisms. In L. A. Matthews, S. M. Cabarcas, and E. Hurt (Eds.), DNA repair of cancer stem cells (pp. 25-26). http://www.springer.com/978-94-007-4589-6.
Cooper, G. M. (2000). DNA repair. In The cell: A molecular approach (2nd ed.). Sunderland, MA: Sinauer Associates. Retrieved from http://www.ncbi.nlm.nih.gov/books/NBK9900/#_A802_.
Dexheimer, T. S. (2013). DNA repair pathways and mechanisms. In L. A. Matthews, S. M. Cabarcas, and E. Hurt (Eds.), DNA repair of cancer stem cells (p. 21). http://www.springer.com/978-94-007-4589-6.
Cooper, G. M. (2000). DNA repair. In The cell: A molecular approach (2nd ed.). Sunderland, MA: Sinauer Associates. Retrieved from http://www.ncbi.nlm.nih.gov/books/NBK9900/#_A799_.
Dexheimer, T. S. (2013). DNA repair pathways and mechanisms. In L. A. Matthews, S. M. Cabarcas, and E. Hurt (Eds.), DNA repair of cancer stem cells (pp. 22-24). http://www.springer.com/978-94-007-4589-6.
Hang, B. (2010). Formation and repair of tobacco carcinogen-derived bulky DNA adducts. Journal of Nucleic Acids, 2010, article ID 709521. http://dx.doi.org/10.4061/2010/709521.
Goodsell, D. (2007). Thymine dimers. In RCSB PDB molecule of the month. Retrieved from http://pdb101.rcsb.org/motm/91.
Dexheimer, T. S. (2013). DNA repair pathways and mechanisms. In L. A. Matthews, S. M. Cabarcas, and E. Hurt (Eds.), DNA repair of cancer stem cells (pp. 26-27). http://www.springer.com/978-94-007-4589-6.
Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., and Walter, P. (2002). DNA repair. In Molecular biology of the cell (4th ed.). New York, NY: Garland Science. Retrieved from http://www.ncbi.nlm.nih.gov/books/NBK26879/#_A840_.
Kimball, J. W. (2015, October 31). DNA repair. In Kimball's biology pages. Retrieved from https://www.biology-pages.info/D/DNArepair.html#DSBs
Lynch syndrome. (2013). In Genetics home reference. Retrieved from http://ghr.nlm.nih.gov/condition/lynch-syndrome.
Da Silva, F. C., Valentin, M. D., Ferreira, F. de O., Carraro, D. M., and Rossi, B. M. (2009). Mismatch repair genes in Lynch syndrome: A review. Sao Paulo Med. J., 127(1), 46-51. http://dx.doi.org/10.1590/S1516-31802009000100010.
Xeroderma pigmentosum. (2010). In Genetics home reference. Retrieved from http://ghr.nlm.nih.gov/condition/xeroderma-pigmentosum.

References:

Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., and Walter, P. (2002). DNA repair. In Molecular biology of the cell (4th ed.). New York, NY: Garland Science. Retrieved from http://www.ncbi.nlm.nih.gov/books/NBK26879/.

Augusto-Pinto, L., da Silva, C. G. R., Lopes, D. de O., Machado-Silva, A., and Machado, C. R. (2003). Escherichia coli as a model system to study DNA repair genes of eukaryotic organisms. Genet. Mol. Res., 2(1), 77-91. Retrieved from http://www.funpecrp.com.br/gmr/year2003/vol1-2/sim0001_full_text.htm.

Base excision repair. (2015, December 8). Retrieved January 23, 2016 from Wikipedia: https://en.wikipedia.org/wiki/Base_excision_repair.

Berg, J. M., Tymoczko, J. L., and Stryer, L. (2002). DNA polymerases require a template and primer. In _Biochemistry (5th ed., section 27.2.4). New York, NY: W. H. Freeman, 2002. http://www.ncbi.nlm.nih.gov/books/NBK22374/#_A3777_.

Cooper, G.M. (2000). DNA repair. In The cell: A molecular approach (2nd ed.). Sunderland, MA: Sinauer Associates. Retrieved from http://www.ncbi.nlm.nih.gov/books/NBK9900/.

Da Silva, F. C., Valentin, M. D., Ferreira, F. de O., Carraro, D. M., and Rossi, B. M. (2009). Mismatch repair genes in Lynch syndrome: A review. Sao Paulo Med. J., 127(1), 46-51. http://dx.doi.org/10.1590/S1516-31802009000100010.

Dexheimer, T. S. (2013). DNA repair pathways and mechanisms. In L. A. Matthews, S. M. Cabarcas, and E. Hurt (Eds.), DNA repair of cancer stem cells (pp. 19-32). http://www.springer.com/978-94-007-4589-6.

DNA mismatch repair. (2015, December 19). Retrieved January 23, 2016 from Wikipedia: https://en.wikipedia.org/wiki/DNA_mismatch_repair.

Endonuclease. (2016, January 24). Retrieved January 25, 2016 from Wikipedia: https://en.wikipedia.org/wiki/Endonuclease.

Exonuclease. (2016, January 24). Retrieved January 25, 2016 from Wikipedia: https://en.wikipedia.org/wiki/Exonuclease.

Goodsell, D. (2007). Thymine dimers. In RCSB PDB molecule of the month. Retrieved from http://pdb101.rcsb.org/motm/91.

Hang, B. (2010). Formation and repair of tobacco carcinogen-derived bulky DNA adducts. Journal of Nucleic Acids, 2010, article ID 709521. http://dx.doi.org/10.4061/2010/709521.

Kimball, J. W. (2015, October 31). DNA repair. In Kimball's biology pages. Retrieved from http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/D/DNArepair.html.

Lynch syndrome. (2013). In Genetics home reference. Retrieved from http://ghr.nlm.nih.gov/condition/lynch-syndrome.

http://www.bioinfo.org.cn/book/biochemistry/chapt24/sim4.htm.

Modrich, P. (2006). Mechanisms in eukaryotic mismatch repair. J. Biol. Chem., 281(41), 30305-30309. http://dx.doi.org/10.1074/jbc.R600022200.

Nucleotide excision repair. (2016, January 2). Retrieved January 23, 2016 from Wikipedia: https://en.wikipedia.org/wiki/Nucleotide_excision_repair.

OpenStax College, Biology. (2015, September 29). DNA repair. In OpenStax CNX. Retrieved from http://cnx.org/contents/30fcb950-c2a6-4dab-b62f-549c8ce3d7d1@6/DNA-Repair.

Pezza, J. A., Kucera, R., and Sun, L. (n.d.). Polymerase fidelity: What is it, and what does it mean for your PCR? In Tools and resources. Retrieved July 28, 2016 from https://www.neb.com/tools-and-resources/feature-articles/polymerase-fidelity-what-is-it-and-what-does-it-mean-for-your-pcr.

Photolyase. (2015, October 8). Retrieved January 23, 2016 from Wikipedia: https://en.wikipedia.org/wiki/Photolyase.

Purves, W. K., Sadava, D. E., Orians, G. H., and Heller, H.C. (2004). DNA proofreading and repair. In Life: The science of biology (7th ed., pp. 227-228). Sunderland, MA: Sinauer Associates.

QIAGEN. (2015). Mismatch repair in eukaryotes. In GeneGlobe. Retrieved from https://www.qiagen.com/us/shop/genes-and-pathways/pathway-details/?pwid=293.

Reece, J. B., Urry, L. A., Cain, M. L., Wasserman, S. A., Minorsky, P. V., and Jackson, R. B. (2011). Proofreading and repairing DNA. In Campbell biology (10th ed., pp. 325-327). San Francisco, CA: Pearson.

Xeroderma pigmentosum. (2010). In Genetics home reference. Retrieved from http://ghr.nlm.nih.gov/condition/xeroderma-pigmentosum.

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krabas
Posted 8 years ago. Direct link to krabas's post “why would cells ever appl...”
why would cells ever apply non-homologous end joining if there is a cleaner and safer alternative? Do they only do that when there's no undamaged template available?
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(38 votes)
Answer
- dasrishov74
  Posted 4 years ago. Direct link to dasrishov74's post “In the absense of homolog...”
  In the absense of homologous chromosome (when DNA hasn't undegone replication yet)
  non homologous end joining is done.
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  (13 votes)
Matthew Winkler
Posted 7 years ago. Direct link to Matthew Winkler's post “Is there potential, durin...”
Is there potential, during any of the above proofreading methods to "correct" the template DNA rather than the newly-formed strand?
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(12 votes)
Answer
- Satwik Pasani
  Posted 7 years ago. Direct link to Satwik Pasani's post “By potential, do you mean...”
  By potential, do you mean that is mistakenly correcting the template strand possible? If so, then yes it is. The mechanism to determine which is the newly-formed and the template strand isn't perfect and relies on methylation and other epigenetic markers. These can fail. If the damage includes these markers, or the damage/defective piece is extensive so as to avoid these markers from being introduced, or if the damage doesn't allow the DNA repair machinery to sense these markers, it is very much possible the correction is faulty. Some repair machineries are anyway strand non-specific, and some are even sequence non-specific (see Non Homologous End Joining, which is the last resort at DNA stability).
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  (14 votes)
pcantu000
Posted a year ago. Direct link to pcantu000's post “Why is thymine in DNA and...”
Why is thymine in DNA and uracil in RNA?
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(7 votes)
Answer
- NadiaElisabeth27
  Posted 10 months ago. Direct link to NadiaElisabeth27's post “Thymine is the nucleotide...”
  Thymine is the nucleotide that DNA uses. RNA is not the same thing as DNA so it seems very natural that the two of them would have some differences. Uracil is one of them.
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  (8 votes)
rokaia 00
Posted 6 years ago. Direct link to rokaia 00's post “what happen if DNA have u...”
what happen if DNA have uracil instead of uracil ? how can DNA repair it ?
and what are the reasons that DNA contain thymine not uracil
Button navigates to signup pageComment on rokaia 00's post “what happen if DNA have u...”
(5 votes)
Answer
- tyersome
  Posted 6 years ago. Direct link to tyersome's post “In your question – "what ...”
  In your question – "what happen if DNA have uracil instead of uracil ?" — I am assuming your second "uracil" was supposed to be "thymine" ...
  
  I'm not sure what you really want to know — as it says in the article, uracil in DNA is usually recognized as a mistake and removed by the Base Excision Repair pathway ...
  
  There are a number of proposed reasons why thymine is used in DNA.
  
  1) Cytosine residues in DNA undergo a spontaneous change that converts them into uracil. There are enzymes that specifically recognize and remove uracil (but not thymine) from DNA and this helps suppress what would otherwise be a major contributor to the rate mutations.
  
  2) Thymine is chemically more stable (though slightly more expensive to make), so this again probably helps reduce the mutation rate.
  
  An interesting and detailed discussion of these factors and more can be found here:
  http://www.scienceinschool.org/2011/issue18/uracil
  
  If you have further questions please leave a comment.
  Comment on tyersome's post “In your question – "what ...”
  (10 votes)
Mia Langer
Posted 5 years ago. Direct link to Mia Langer's post “When the base correcting ...”
When the base correcting processes take the damaged bases away, where do they go so that they are not harmful to the body?
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(6 votes)
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Raymundo Hiragane
Posted 7 years ago. Direct link to Raymundo Hiragane's post “In the Mismatch repair, w...”
In the Mismatch repair, why is a section of DNA cut off rather than only the mismatched base pair cut off?
Button navigates to signup pageComment on Raymundo Hiragane's post “In the Mismatch repair, w...”
(5 votes)
Answer
- poshlost
  Posted 6 years ago. Direct link to poshlost's post “So it depends on the mech...”
  So it depends on the mechanism used. Base excision repair only removes one base (deaminated cytosine for example). Nucleotide excision repair is used with thymine dimers when the DNA is warped, and in that case it removes a 12-24 nucleotide section. Generally proteins are not very wasteful.
  Button navigates to signup page
  (2 votes)
myerrid
Posted 6 years ago. Direct link to myerrid's post “What occurs in cancerous ...”
What occurs in cancerous cells when going through mismatch repair? Is the issue ignored? Or is it because the cancerous cell had gone through mismatch repair, then became cancerous?
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(4 votes)
Answer
- poshlost
  Posted 6 years ago. Direct link to poshlost's post “In cancer cells, the mism...”
  In cancer cells, the mismatch repair has not happened. This leads to mutations. This is a classic example: https://en.wikipedia.org/wiki/Xeroderma_pigmentosum Without the nucleotide excision repair system, the individual develops melanoma and/or carcinoma at a very young age. Also recall that skin cancer metastasizes to the lungs, so this is a very bad prognosis indeed.
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  (3 votes)
samantha tam
Posted 3 years ago. Direct link to samantha tam's post “Why is thymine in DNA and...”
Why is thymine in DNA and uracil in RNA?
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(2 votes)
Answer
- YDW Mv!k0m
  Posted 3 years ago. Direct link to YDW Mv!k0m's post “Uracil is the cheapest to...”
  Uracil is the cheapest to produce energetically, and is therefore favored at the RNA level where fidelity is not as important and large quantities are produced.
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  (7 votes)
Faiq
Posted 7 years ago. Direct link to Faiq's post “How the proteins involved...”
How the proteins involved in DNA repair detect the fault?
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(4 votes)
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- RowanH
  Posted 4 years ago. Direct link to RowanH's post “It depends on what is wro...”
  It depends on what is wrong. For example, some damage distorts the shape of the DNA helix, and there are proteins scanning the genome for this. Sometimes damage is detected when an RNA polymerase stalls. In mismatch repair, there are proteins involved that detect the mismatch, and proteins that detect which is the old and which is the newly synthesised DNA strand.
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  (3 votes)
ethical313
Posted 4 years ago. Direct link to ethical313's post “why is rna primer even re...”
why is rna primer even required if the dna polymerase III will introduce the nucleotide bases complementary to the leading or lagging strand?
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(3 votes)
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- Ivana - Science trainee
  Posted 4 years ago. Direct link to Ivana - Science trainee's post “The synthesis of a primer...”
  The synthesis of a primer is necessary because the enzymes that synthesize DNA, which is called DNA polymerases, can only attach new DNA nucleotides to an existing strand of nucleotides.
  
  https://www.nature.com/scitable/definition/primer-305/
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  (1 vote)