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Why does DNA mutate?

Why does DNA mutate?


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I just read that pregnancy in space would be super dangerous because - among other reasons - of a higher risk of mutations due to radiation. This made me wonder: why does the DNA in organisms mutate? What are the main natural reasons? Is this due to the construction of DNA and would happen even in "perfect" conditions or is it due to something that is in the environment, like radiation?

So far I got two answers on reddit and also asked this question to a doctor and what I heard is along the lines of "this is how it is". I heard about "cells being worn out". But what makes the process non-deterministic, probabilistic? I guess I don't know enough about biochemistry to formulate the question, but I guess it's related to "given certain conditions, what determines at which point (and what kind of) a mutation occurs?"


If I am not mistaken, the vast majority of mutations happen during DNA replication.

DNA must replicate itself so that cells can replicate itself. The DNA polymerase is one very important protein that replicates DNA. The human genome (to consider this example) is 3.5 billions nucleotides long. Just to realize how long is 3.5 billions letters, let's make a book analogy.

Book analogy

  • In the Harry Potter series, there are about one million words (ref).
  • In the LOTR series, there are about one 400 thousands words (ref).
  • In the Chronicles of Narnia series, there are about 230 thousands words (ref)
  • In the King James Bible, there are about 788 thousands words (ref)

This sums to about 2.4 millions words. As, in english, there are 5.1 letters on average per word (ref), this lead to a total of about 12.3 millions letters. Imagine you have to rewrite all of these books almost 300 times (12.3 millions * 300 ≈ 3.5 billions)! How many typos would you make?

There are several cell divisions between a zygote and the ovule/spermatozoid produced by this individual but as most mutations happen during meiosis, I will just ignore mitotic mutations. The DNA polymerase makes about one typo every 100 millions nucleotides (Kong et al. 2012; Rahbari et al. 2016)! So really, the DNA polymerase is doing a pretty good job!

What is causing mutations?

Shit happens

I am hoping that form the above analogy, you may have a sense that mutations are just small mistakes. They happen because the replicating machinery is not perfect. Sometimes a molecule comes sideway, does not bind very well and another molecular passing by sticks to the DNA, etc… Errors happen just like you would be making a lot of typos, rewriting books.

Mutagens

There are of course factors that can affect this mutation rate. Physical, chemical and biological agents increasing the mutation rate are called mutagens and they include radiation decay, ultraviolet radiation, ROS, benzene as well as some viruses and some parasitic bacteria.

Variation along the genome

Note also that the mutation vary along the genome too. Regions with high repeats (e.g.AATAATAATAATAATAATAATAAT) such as microsatellites for example tend to have a much higher mutation rate.

Variation among species and Drake's rule

Mutation rate also vary among species. There is a general tendency that the per nucleotide mutation rate negatively covary with the genome size, a phenomenon called Drake's rule (see for example Bradwell et al. 2013 or one of the early Drake's paper).


Short answer, Chemistry runs off probability, and life and DNA replication are in the end chemical reactions.

DNA is a chemical, and the bonds between different nucleotides sequences are all extremely similar, if there was not an opposing strand, mutations would be extremely common becasue any sequence is essentially equally energetically favorable,(AKA equally likely probabilistically/chemically). Having two joined strands means you cant just swap nucleotides becasue they can't bond across strands equally well, there is a heavy chemical bias for only bonding with the opposing partner. A=T C=GT. Any other bond is less energetically favorable ( AKA less likely, which is not the same thing as impossible). The dual strand nature of DNA makes errors less likely but we are still talking chemistry and no chemical process is absolutely perfect, even if you burn carbon and oxygen in perfect ratios to get CO2 you will still get CO, carbon monoxide, just do to the physical (and thus probabilistic) nature of chemical reactions. Even the strength of the bond between the two stands can work against it as f a mutation does slip in the DNA will still hold together, and if it gets replicated before an error correcting mechanism catches it it will stick around. The kicker is although a DNA is very unlikely to mutate, there is a lot of it so even the extremely unlikely still occurs, DNA also has to be split apart to be replicated, during which mutations are far less energetically unfavorable.

Cells actually have dozens of error checking mechanisms and chemical stabilizers to limit how many of these can get through or occur however again this is a physical chemical process, thus it will not be perfect. Even without these mechanisms DNA replications is still fairly reliable, but many organisms have gigantic genomes meaning even reliable as a swiss watch is still not good enough. It is simply impossible to create a perfect copying mechanism that has high turnover that operates in the real world there are just to many interactions. the fact many replications are happening at once does not help since sometimes these many disjointed strands can end up bonding together causing the error correcting mechanisms to cut out entire sections, or mix them up trying to fix it.


Mutations occur due to sudden and unpredictable changes in the structure of DNA. Radiations, particularly those of energies of ultraviolet and higher are capable of breaking the bonds that make up DNA. This fragments the DNA. While DNA has mechanisms to counter this, and reform as a complete strand, it's not perfect and the original DNA might not be made. Oftentimes, a small error such as base pair swaps or a missing pair could occur. These changes are reflected as mutations.


As ultraviolet radiation forms thymine diamers due to free radical addition reactions, this is one of the environmentatally caused damage to DNA. There are various mutagens which do the same. Since DNA is a chemical molecule the fate of any chemical molecule is the tendency to undergo changes, even during normal conditions chemical reactions occur. Take for example the transformation caused by deamination of cytosine residues which changes it into uracil or deamination of adenine to form hypoxanthine. Another important reaction is hydrolysis of glycosyl bonds between sugar and nucleotides creating a DNA lesion more commonly called depurination. 10000 purines are estimated to be lost in 24 hrs in mammalian cells increasing concentration of acids by any random mechanism might also accelerate the depurination process. So DNA like any chemical material is subjected to changes though there are processes to check this process still it happens. Moreover during replication there are practical chances of error in spite of various check points. Depending upon the chemistry of the reaction DNA is undergoing at which point a mutation would occur might be studied, numerous biochemical process takes place simultaneously further complicates the precise location where a mutation might take place.


Why does DNA mutate? - Biology

You’re one of a kind. It’s not just your eyes, smile, and personality. Your health, risk for disease, and the ways you respond to medicines are also unique. Medicines that work well for some people may not help you at all. In fact, they might even cause problems. Wouldn’t it be nice if treatments and preventive care could be designed just for you?

The careful matching of your biology to your medical care is known as personalized medicine. It’s already being used by health care providers nationwide.

The story of personalized medicine begins with the unique DNA you inherited from your parents. DNA is responsible for all the physical traits that make you function as a human organism. It plays a vital role in life on this planet. DNA stores genetic information.

Genes are stretches of DNA that serve as a sort of instruction manual telling your body how to make the proteins and perform the other tasks that your body needs. The same genes often differ slightly between people. Bases may be switched, missing, or added here and there. Most of these variations have no effect on your health. But some can create unusual proteins that might boost your risk for certain diseases. Some variants can affect how well a medicine works in your body. Or they might cause a medicine to have different side effects in you than in someone else.

It’s becoming more common for doctors to test for gene variants before prescribing certain drugs. “If doctors know your genes, they can predict drug response and incorporate this information into the medical decisions they make,” says Dr. Rochelle Long, a pharmacogenomics expert at NIH. “By screening to know who shouldn’t get certain drugs, we can prevent life-threatening side effects,” Long says.

Even one of the oldest and most common drugs, aspirin, can have varying effects based on your genes. Millions of people take a daily aspirin to lower their risk for heart attack and stroke. Aspirin helps by preventing blood clots that could clog arteries. But aspirin doesn’t reduce heart disease risk in everyone.

Personalized Medicine in Practice

Here are just a few treatments that benefit from personalization:

So what does this mean for you? Is personalized medicine something you should look into? Let’s learn more about DNA and genetics to see if we can answer this question.


What is DNA?

DNA (Photo Credit : Forluvoft / Wikimedia Commons)

DNA is the abbreviated name for deoxyribonucleic acid, a biomolecule. Adenine (A), Thymine (T), Cytosine (C), and Guanine (G) are the 4 monomers (nucleotides) that combine to form DNA. What holds all these monomers in the sequence is the phosphate backbone structure. Now, unless you&rsquore familiar with biology, you might not really understand what I&rsquom rambling on about.

Putting it in even simpler words, DNA is why you got your mother&rsquos eye color or your dad&rsquos hair color, because DNA stores all the genetic information. Heredity exists because you have the DNA that stores all the features of your parents!


Both long and short wavelength UV light are damaging to DNA, but in different ways. Short wavelength UV-B and UV-C light can directly cause dimerization of pyrimidines, and directly prevent replication of plasmid DNA, or induce mutations after faulty repair. Long wavelength UV-A light is generally less directly damaging, and instead causes mutations through the production of reactive oxygen species. In the lab, UV-A is less harmful to naked DNA. This is why it is best to use a long-wavelength transilluminator to visualize DNA bands, if possible! However, with enough exposure, UV-A light could still damage your DNA.

Hopefully this article has not only taught you the importance of using a broad-spectrum sunscreen, but also taught you the chemistry behind the damaging effects of UV light. What other questions do you have about UV light or DNA mutations?


How Can Mutations In Mitochondrial DNA Affect The Human Body?

What are some of the disease symptoms that can result from a mutation in the mitochondrial DNA? originally appeared on Quora: the place to gain and share knowledge, empowering people to learn from others and better understand the world.

Answer by Suzanne Sadedin, Ph.D. in evolutionary biology, on Quora:

Mitochondrial mutations can cause several syndromes (groups of symptoms), which may be distinct or overlap. Symptoms in a syndrome tend to co-occur, but most individuals will not experience all symptoms associated with the syndrome. In addition, symptoms can vary dramatically from one individual to another, even with the same mutation*. Because mitochondria are responsible for ATP production, the organs most affected are often those with high energy demand, such as the brain, muscles and heart. In addition, tissues where there is little cell turnover (like the brain) are more often affected because selection on cell lineages favors those with fewer mitochondrial mutations.

Syndromes include MELAS, MERRF, Leigh, Kearns-Sayre, Leber’s hereditary optic neuropathy, and maternally inherited diabetes and deafness.

MELAS is caused by defects in mitochondrial tRNA Leu(UUA/UUG) (A3243G in around 80% of cases, and T3271C in

7.5% of cases many other rare mutations can have the same effect). Its most common symptoms include:

  • Stroke-like episodes, usually starting at a young age, leading to progressive loss of motor abilities, vision, hearing and cognitive ability.
  • Seizures (often with temporary unilateral paralysis, blindness or altered consciousness).
  • Frequent headaches / migraines.

MERRF is most commonly caused by mutations in MT-TK, but can also result from mutation to MT-TL1, MT-TH, and MT-TS1 in the latter cases, symptoms of other syndromes usually co-occur. Symptoms include:

  • muscle twitches, weakness and stiffness
  • recurrent seizures
  • loss of coordination
  • loss of sensation in extremities
  • loss of sight and hearing
  • dementia
  • short stature
  • heart disease
  • lipomas

Leigh syndrome is more often caused by nuclear mutations, but results from mitochondrial mutations in about 20% of cases (most commonly, a mutation to MT-ATP6). Symptoms usually (but not always) appear in infants, starting with vomiting, diarrhea, and difficulty swallowing, leading to failure to thrive. Muscle weakness and movement problems, loss of sensation, paralysis of eye muscles and loss of vision often follow. Severe breathing problems worsen over time death within 2–3 years is typical.

Kearns-Sayre syndrome results from a large, single mitochondrial deletion, most commonly of 4997 nucleotides (12 genes). This is usually a somatic mutation, not an inherited one (I guess it’s lethal in early embryos). Its primary symptom is weakness and paralysis of the eye muscles and blindness it can also cause deafness, heart abnormalities, endocrine problems, problems with coordination and balance, muscle weakness, kidney failure, dementia and diabetes.

Leber’s hereditary optic neuropathy is caused by a point mutation in ND4, ND1 or ND6 subunit gene of complex I. It causes abrupt loss of sight in first one eye, then the other, usually in early adulthood.

*Symptoms vary. This variation has important consequences for patients and families:

  • Symptoms may not be evident in every generation or sibling, even when the disorder is inherited.
  • Testing for inheritance is tricky. When the family is asymptomatic, genetic testing can show that the disorder is inherited, but it can’t show that the disorder is not inherited. That is, if one or more maternal line family members tests positive for the same mutation as the patient, you can probably assume the entire maternal line are carriers. But even if they all test negative, they might still be carriers.
  • Symptoms can affect different organ systems in different individuals, even when those individuals share the same mutation. This means that family members can have diseases that seem unrelated, but are actually caused by the same mitochondrial mutation.
  • Symptoms can appear at any age all are often seen in young people, and certain ages are more typical for certain syndromes.

Why do the symptoms of mitochondrial disease vary so much? There is a great deal we don’t know about these diseases, and some of what we think we know may turn out to be wrong.

The standard answer to this question is heteroplasmy: different versions of the mitochondrial genome can coexist in each cell. Each cell contains thousands of copies of mitochondrial DNA. These copies reproduce asexually within the cell, so the proportion of mutants in any one cell changes over time. Moreover, each mitochondrion can contain several copies, allowing it to function normally even when some copies are mutated. The result of this is that cells can carry very high loads of mutant mitochondrial DNA (up to 90%) before their function is affected. So disease symptoms emerge only when the mutant load exceeds a threshold.

Compared with nuclear DNA, mitochondrial DNA is at least 10 times more vulnerable to mutation. Within the lifetime of an individual, mitochondrial mutations accumulate. This may result in a gradual decline in many different cellular metabolic functions. In fact, some researchers believe that mitochondrial failure is a primary cause of aging.

Cell division uses a lot of ATP, so cell lineages with a high proportion of mutant mitochondria tend to be uncompetitive. Consequently, in tissues with rapid cell turnover, mitochondrial mutations are (usually) relatively suppressed (presumably until they approach the Hayflick limit, the number of divisions after which cells must stop dividing). In contrast, in tissues where cells don’t often divide (like neurons) mutations accumulate more rapidly.

Mutant mitochondria are purged by selection among cell lineages, especially via a population bottleneck that occurs during early development. In mice (and likely other mammals as well), for a few days after fertilization, the zygote’s cells divide, but mitochondria do not. So each cell ends up with a small subset of the mitochondria that were present in the zygote. It’s believed these cells then compete metabolically those that have a relatively high proportion of mutant mitochondria are mostly eliminated because they are unable to generate energy efficiently.

Whilst this bottleneck on average reduces the mutation load of the offspring below that of the mother, some proportion of mutant mitochondria can still survive. And if the specific cell lineage that gave rise to the mother’s ova happened to have a high mutant load, then her offspring may still have a higher load than she does.

Moreover, the symptoms and age when a mitochondrial disorder appears depends on the concentration of mutations within the particular cell lineage that gives rise to an organ system during development. As a result the same mutation might in one individual cause (for example) diabetes at 20, in another seizures and stroke at 46, whilst a third might have no noticeable symptoms ever.

However, heteroplasmy can’t be the full story. Most of the genes that build and control mitochondria have been outsourced to the nuclear genome (which makes sense, because the nuclear genome has much better control over mutations). So the expression of disorders that affect mitochondrial function can also be directly influenced by autosomal genes. But these autosomal diseases that impair ATP production are also immensely variable in their expression, even though they don’t involve heteroplasmy. We don’t know why this is yet. Gene interactions are complex, and we have yet to untangle even a tiny minority of them.

DISCLAIMER: I’m not a medical doctor. This is just my understanding of current knowledge based on reading research papers. If you need a diagnosis, talk to your doctor. The symptoms of mitochondrial disorders vary wildly and are usually shared with many other diseases you can’t diagnose yourself based on symptoms alone.

Some useful sources below:

This question originally appeared on Quora. the place to gain and share knowledge, empowering people to learn from others and better understand the world. You can follow Quora on Twitter, Facebook, and Google+. More questions:


Clinical Significance

Antibiotic Resistance

Antibiotics work through a variety of mechanisms:[17]

When an antibiotic loses theꃊpacity to kill or control bacterial growth, antibiotic resistance occurs. This can occur in two ways:

These circumstances exacerbate under selective pressure (i.e., the use of antibiotics). Antibiotic resistance can spread both vertically and horizontally through a population. Horizontal transfer is considered the primary mediator of antibiotic resistance. The following are non-comprehensive examples of how two of the classes of antibiotics mentioned above encounter resistance mutations.

DNA Synthesis Inhibitor

In gram-negative bacteria, such as Helicobacter pylori, mutation resistance occurs relatively quickly to fluoroquinolones and thereby poses clinical issues for these therapies. Levofloxacin, moxifloxacin, and ciprofloxacin, examples of fluoroquinolones, inhibit DNA synthesis by targeting two homologous enzymes (DNA topoisomerase II and IV).[18] These enzymes are necessary for the supercoiling of bacterial DNA.  

Gram-negative bacterial resistance to fluoroquinolones includes the accumulation of substitution mutations in the coding regions for particular subunits of DNA topoisomerase II. Resistance can be enhanced further by efflux pump modification.[19]਌iprofloxacin targets only the parC subunit while other quinolones target one or more of these subunits.[20]ਏor example, garenoxacin targets both DNA topoisomerases II and IV thus is less prone to resistance. Resistance to Garenoxacin requires both proteins to have resistance mutations.[21]

Combination therapy for Helicobacter pylori typically includes clarithromycin (protein synthesis inhibitor), metronidazole (DNA synthesis inhibitor), amoxicillin (Cell wall synthesis inhibitor), or tetracycline (protein synthesis inhibitor), and a proton pump inhibitor.[22][23][24]

Protein Synthesis Inhibitor

Linezolid prevents protein synthesis and is active against resistant Gram-positives.[25] Linezolid inhibits the formation of the 70S ribosomal initiation complex through binding to the 23S portion of the 50S subunit.[26] Infrequent resistance found in strains of S.ਊureus,ਊnd coagulase-negative staphylococci has mutations in the central loop of the domain V region of the 23S rRNA gene. More specifically,਌linical isolates had a substitution of Thymine for Guanine at the 2576 position.[27][28]

Intrinsically, resistant bacteria have a characteristic resistance within all members of a species or genus. Such resistance may arise because:

Antibiotic resistance mechanisms can also occur by incorporating resistance genes into plasmids, transposons, and integrons. These genes spread through horizontal transfer by conjugation, transformation, or transduction mechanisms. However, the mutation is essential for the evolution or assortment of these genes.


What is meant by the term "degenerate" when describing DNA? Why does it occur and what are its implications for protein structure?

"Degenerate" refers to redundancy in the genetic code. Amino acids, the building blocks of proteins, are encoded by codons of three nucleotide bases. Some amino acids are encoded by more than one codon, for example glutamic acid (GAA and GAG). Degeneracy occurs because there are more codons than amino acids. If codons were composed of two bases, this means there would only be 16 amino acids encoded (4^2 = 16). However, there are 21 amino acids and so codons are formed by three bases (4^3 = 64), meaning there must be some redundancy in the code.

Degeneracy means a mutation altering one base in a codon is unlikely to alter the amino acid structure of the encoded protein, because the codon is likely to still encode the same amino acid. This makes the genetic code more fault-tolerant to point mutations.


Multiple Choice

Which of the following is a change in the sequence that leads to formation of a stop codon?

A. missense mutation
B. nonsense mutation
C. silent mutation
D. deletion mutation

The formation of pyrimidine dimers results from which of the following?

A. spontaneous errors by DNA polymerase
B. exposure to gamma radiation
C. exposure to ultraviolet radiation
D. exposure to intercalating agents

Which of the following is an example of a frameshift mutation?

A. a deletion of a codon
B. missense mutation
C. silent mutation
D. deletion of one nucleotide

Which of the following is the type of DNA repair in which thymine dimers are directly broken down by the enzyme photolyase?

A. direct repair
B. nucleotide excision repair
C. mismatch repair
D. proofreading

Which of the following regarding the Ames test is true?

A. It is used to identify newly formed auxotrophic mutants.
B. It is used to identify mutants with restored biosynthetic activity.
C. It is used to identify spontaneous mutants.
D. It is used to identify mutants lacking photoreactivation activity.


DNA Mutations

DNA mutations are permanent changes in the DNA sequence of a gene. Mutations range in their severity. Some damage the way a cell or whole organism functions, or even cause lethality, while others have no effect. Mutations also range in the amount of DNA altered. They can involve from a single nucleotide up to large segments of chromosomes. DNA mutations can be:

Image Courtesy of Wikimedia Commons

* Inherited: parents that have mutations can pass them to their offspring.
* Germ line mutations: are present in every cell of an individual, including the egg or sperm used in the production of offspring.
* De novo (new) mutations: occur by chance in one or a few eggs or sperm, or just after fertilization, and are NOT present in every cell of a parent. These explain situations where a child has a genetic disorder that is unseen in the family history.
* Acquired: environmental agents, called mutagens, can alter DNA. An example of a common mutagen are the UV wavelengths in sunlight associated with skin cancer (see image). Acquired mutations are typically not passed to offspring but can be if they alter DNA sequences in egg or sperm.

* Insertion/Duplication/Deletion: the addition or subtraction of nucleotides from DNA sequence. They can be as small as single nucleotides or large enough to visualize on a chromosome and involve tens to hundreds of thousands of nucleotides.
* Point Mutation: the change in one nucleotide for another. For example, an “A” becomes a “T”.
* Translocation: the movement of a segment of DNA from one chromosome to another.
* Inversion: the 180° flip of a DNA segment so that that it is reversed compared to the original structure.

Ultimately whether or not a particular mutation causes a detrimental effect is due to the location of the mutation within a gene (or genes) as well as the significance of that gene’s function.


How Does DNA Polymerase Prevent Mutations

DNA polymerase is the enzyme responsible for the addition of nucleotide bases to the growing strand during DNA replication. Since the nucleotide sequence of a genome determines the development and functioning of a particular organism, it is vital to synthesize the exact replica of the existing genome during DNA replication. Generally, DNA polymerase maintains high fidelity during DNA replication, only incorporating single mismatched nucleotide per 10 9 added nucleotides. Therefore, if a mispairing occurs between nitrogenous bases in addition to the standard complementary base pairs, DNA polymerase add that nucleotide to the growing chain, producing a frequent mutation. The errors of DNA replication are corrected by two mechanisms known as proofreading and strand-directed mismatch repair.

Proofreading

Proofreading refers to an initial mechanism of correcting the mispairing base pairs from the growing DNA strand, and it is carried out by DNA polymerase. DNA polymerase carries out proofreading in two steps. The first proofreading occurs just before the addition of a new nucleotide to the growing chain. The affinity of correct nucleotides for DNA polymerase is many times higher than that of the incorrect nucleotides. However, the enzyme should undergo a conformational change just after the incoming nucleotide binds to the template through hydrogen bonds but, before the covenant binding of the nucleotide to the growing strand by the action of DNA polymerase. The incorrectly-base paired nucleotides are prone to dissociate from the template during the conformational change of the DNA polymerase. Hence, the step allows DNA polymerase to ‘double-check’ the nucleotide before adding it to the growing strand permanently. The proofreading mechanism of DNA polymerase is shown in figure 2.

Figure 2: Proofreading

The second proofreading step is known as exonucleolytic proofreading. It occurs immediately after the incorporation of a mismatched nucleotide to the growing strand in a rare instance. DNA polymerase is incapable of adding the second nucleotide next to the mismatched nucleotide. A separate catalytic site of the DNA polymerase known as 3′ to 5′ proofreading exonuclease digests the mispaired nucleotides from the growing chain.

Strand-Directed Mismatch Repair

Despite proofreading mechanisms, DNA polymerase may still incorporate incorrect nucleotides to the growing strand during DNA replication. The replication errors that have escaped from proofreading are removed by the strand-directed mismatch repair. This system detects distortion potential in the DNA helix that is due to mismatched base pairs. However, the repair system should identify the incorrect base from the existing base prior to replacing the mismatch. Generally, E. coli depends on DNA methylation system to recognize the old DNA strand in the double helix as the newly-synthesized strand may not undergo DNA methylation soon. In E.coli, the A residue of the GATC is methylated. The fidelity of the DNA replication is increased by an additional factor of 10 2 due to the action of strand-directed mismatch repair system. The DNA mismatch repair pathways in eukaryotes, bacteria, and E. coli are shown in figure 3.

Figure 3: DNA Mismatch Repair in Eukaryotes, Bacteria, and E. coli

In the strand-directed mismatch repair, three complex proteins move through the newly-synthesized DNA strand. The first protein known as MutS detects and binds to the distortions in the DNA double helix. The second protein known as MutL detects and binds to the MutS, attracting the third protein known as MutH that distinguish the unmethylated or the newly-synthesized strand. Upon binding, the MutH cuts the unmethylated DNA strand immediately upstream to the G residue in the GATC sequence. An exonuclease is responsible for the degradation of strand downstream to the mismatch. However, this system degrades regions less than 10 nucleotides that are readily re-synthesized by DNA polymerase 1. The Mut proteins of eukaryotes are homologous to that of E. coli.

Conclusion

Mutations are permanent alterations of the nucleotide sequence of the genome that may arise due to the errors in DNA replication or due to the effect of external mutagens. The errors of DNA replication can be corrected by two mechanisms known as proofreading and strand-directed mismatch repair. Proofreading is carried out by DNA polymerase itself during the DNA synthesis. The strand-directed mismatch repair is carried out by Mut proteins just after the DNA replication. However, these repair mechanisms are involved in the maintenance of the integrity of the genome.

Reference:

1. Alberts, Bruce. “DNA Replication Mechanisms.” Molecular Biology of the Cell. 4th edition., U.S. National Library of Medicine, 1 Jan. 1970, Available here.
2. Brown, Terence A. “Mutation, Repair and Recombination.” Genomes. 2nd edition., U.S. National Library of Medicine, 1 Jan. 1970, Available here.

Image Courtesy:

1. “Different Types of Mutations” By Jonsta247 – This file was derived from:Point mutations-en.png (GFDL) via Commons Wikimedia
2. “DNA polymerase” By I, Madprime (CC BY-SA 3.0) via Commons Wikimedia
3. “DNA mismatch repair” By Kenji Fukui – (CC BY 3.0) via Commons Wikimedia

About the Author: Lakna

Lakna, a graduate in Molecular Biology & Biochemistry, is a Molecular Biologist and has a broad and keen interest in the discovery of nature related things