1. What would happen if a histone was damaged? How would that affect the DNA? 2. Is the same DNA polymerase used for the whole strand of DNA? or do different polymerases switch off? 3. Are there different types of nucleosomes?
To answer your third question, I can find no mention of more than one type of nucleosomes. This doesn't mean that they don't exist, but it is likely that they don't exist.
To answer your second question, On the leading strand the same DNA Polymerase is used throughout the replication process and the lagging strand as it takes place at the replication fork.
For your first question, from what I can find histone damage is either uncommon or not researched as I couldn't find anything specific to that. If a histone was damaged, whatever force caused it would likely damage the cell as a whole. I could find information on decreased histone production, which leads to increased risk of genetic damage and increased transcription rates. It was observed that areas that usually have high nucleosome density stayed the same, while areas with low nucleosome density decreased, most likely because those genes were in some way not as valuable as those which were more highly protected. https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001098#:~:text=Cells%20that%20lack%20proteins%20required,genetic%20damage%20and%20early%20death.
To answer your question, They finish at the exact same time as the lagging strand moves much quicker during replication. Citation https://www.nature.com/articles/nrm2828
For your second question, the purpose of nucleosomes is to aid in the process of supercoiling. DNA strands wrap around histones, creating nucleosomes, which are a core of 8 total histones, 4 pairs of the same. Nucleosomes are soiled into supercoils, which are them coiled into chromosomes. (Textbook)
To answer your third question, non-coding DNA acts as a regulatory system for when and where genes should be turned on or off. https://medlineplus.gov/genetics/understanding/basics/noncodingdna/
For your first question I found from Oregon state that the lagging strand is looped out in such a way that it can be made at the same time as the leading strand. http://oregonstate.edu/instruction/bi314/fall11/dnarep.html#:~:text=How%20can%20both%20leading%20and,direction%20of%20leading%20strand%20synthesis%3F&text=The%20lagging%20strand%20is%20looped,time%20as%20the%20leading%20strand.
How many steps are there is supercoiling? Is the leading strands replication faster than the lagging strand or do they end up at the same speed? Where did the name Okazaki fragments come from?
To answer, your second question, the leading strand does go faster than the lagging strand because the lagging strand has to repeatedly go back and forth, whereas, the leading strand goes forward.
For your third question, I found that Okazaki was the man who discovered the way in which the lagging strand of DNA is replicated in fragments, therefore they are named Okazaki fragments.
To supplement the answers for your third question here is an article about Reji Okazaki and Tsuneko Okazaki and their discovery of Okazaki fragments: https://thebumblingbiochemist.com/365-days-of-science/tsuneko-okazaki-and-the-discovery-of-okazaki-fragments-also-what-those-are/
For your 1st question here is a BioNinja page about supercoiling: https://ib.bioninja.com.au/higher-level/topic-7-nucleic-acids/71-dna-structure-and-replic/supercoiling.html
1. How were Okazaki Fragments discovered? 2. Why did DNA replication evolve in the 3' to 5' manner? 3. What are some ways that Histone could have evolved?
To answer your first question, Okazaki took E. coli and treated them with alkali to separate the hydrogen bonds. After sucrose density gradient centrifugation, the DNA was separated by weight and identified by a radiation test. This proved the concept of a lagging strand because the okazaki fragments were found at the top and the whole DNA was found at the bottom. As time went on the DNA at the top disappeared and the DNA at the bottom grew in quantity. This means that the Okazaki fragments were bonding, meaning that that is how the lagging strand replicates, in fragments.
In response to your second question, the reason that DNA replication evolved as 3 prime to 5 prime is largely due to the proof reading of the created strand. If DNA replicated 5 prime to 3 prime there would be a problem when a misplaced nucleotide was taken out. Once that nucleotide was taken out there would be no way for a replacement to be put in the empty area as no high-energy bond will be broken to provide energy for polymerization. SO, the biggest reason that DNA replication evolved in the 3 prime to 5 prime manner is due to the amount of energy needed for DNA replication from 3 prime to 5 prime being much lower than from 5 prime to 3 prime.
1) What are supernatants? 2) When diffraction occurs, is there a certain or similar pattern they could fall into or is the way it scatters so there is no similarity, this being without using crystals? 3) What are proteins similar to histones?
To answer your first question, supernatants is the soluble liquid reaction after being centrifuged. Citation: https://www.genscript.com/molecular-biology-glossary/11520/Supernatant
To answer your third question, nonhistone proteins that have the function of scaffolding the DNA are similar to histones. Citation:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4889822/
To supplement the answers for your 1st question here is a definition from the Oxford Dictionary: https://www.oxfordreference.com/view/10.1093/oi/authority.20110803100543158
1. Does using a blender to separate the phage from the bacteria always work? 2. Is it possible for there to be an error in the DNA where the Cytosine doesn't pain up with Guanine? 3. Continuing off from question 2, what are the effects of this error if the cell doesn't take notice of it?
For your second question, this is possible and is the main reason errors occur, due to a process called tautomerization, which causes electrons to rearrange and allow for incorrect base pairings. https://www.sparknotes.com/biology/molecular/dnareplicationandrepair/section3/#:~:text=Errors%20in%20DNA%20replication%20can,by%20a%20process%20called%20tautomerization.
In response to question 3, if the mismatched base pair is not noticed by any error correcting component, it becomes a permanent mutation within the cell that carries over to the offspring, thus the effects depend on the type of gene encoded by the mutation. https://www.nature.com/scitable/topicpage/dna-replication-and-causes-of-mutation-409/
Question 1- I tried to find information on other ways to separate the two and if the blender didn't always work but couldn't find much. Most of it was about cultures such as with yeast production being infected and being sure all the phage was gone. I think the blender should always work, I don't think the phage is strong enough to hold onto the bacteria or pellet.
Question 1- Topoisomerase is an enzyme that binds to DNA and cuts the phosphate backbone of one or both strands. https://www.sciencedirect.com/topics/neuroscience/topoisomerase
Question 3- There are three kinds of DNA polymerase, they are called DNA polymerase I, II, and III. Here's a short website that defines the function of each one! https://teaching.ncl.ac.uk/bms/wiki/index.php/DNA_polymerase
Question 2- Sometimes a chromosome doesn't get copied because there is a small stretch of DNA that doesn't get covered by Okazaki fragments. I'm including this link to a Khan Academy lesson that will probably explain it much better than I can :) https://www.khanacademy.org/science/biology/dna-as-the-genetic-material/dna-replication/a/telomeres-telomerase
1) What is the function of heterochromatin? 2) What is the function of telomeres? 3) What would happen if DNA ligase didn't exist? How would the Okasaki fragments be affected?
In response to your second question, the function of telomeres is to prevent genes from being deleted at the end of a chomosome. This is due to the fact that enzymes like DNA polymerase cannot copy DNA all the way to the end of the strand and must stop early. If there were no telomeres then the genes would slowly be destroyed with every replication, instead the repeating codes of telomeres are cut off and do not efect any genes.
Allot, Andrew, and David Mindroff. Biology. Oxford University Press, 2014, p. 351.
In response to question 3, if DNA Ligase didn't exist in a cell, the Okazaki fragments would be unable to connect together, and the DNA molecule would remain incomplete, nullifying it's job within the cell.
1. Is there an enzyme that brings nucleotides to DNA polymerase to use in replicating DNA? 2. Are there examples of organisms running out telomeres? If so, what happened to them? 3. What is the difference between DNA topoisomerase and gyrase?
In regards to your second question, an enzyme called primase aids dna polymerase with replication. Primase makes an RNA primer, or short stretch of nucleic acid complementary to the template, that provides a 3' end for DNA polymerase to work on. For more in depth information, the source i used was https://www.khanacademy.org/science/ap-biology/gene-expression-and-regulation/replication/a/molecular-mechanism-of-dna-replication#:~:text=Primers%20and%20primase,of%20an%20existing%20DNA%20strand.&text=The%20problem%20is%20solved%20with,DNA%20polymerase%20to%20work%20on.
Question 1- the nucleotides are "free" and are within the cytoplasm. These free nucleotides actually come from old mRNA that has been broken down. I could not find any information on any sort of additional enzyme or protein used to bring the nucleotides to the DNA polymerase. I believe they are just free floating and accessible to use as needed. https://mi01000971.schoolwires.net/cms/lib/MI01000971/Centricity/Domain/519/transcription%20pogil%20answers.pdf
In response to your first question, I do not believe that there is a specified enzyme that brings nucleotides to DNA polymerase; DNA polymerase, being an enzyme itself, may just obtain the nucleotides themselves. I apologize, I was unable to find much on this subject. Below is an extra source on DNA polymerase specifically, hope this helps!
1. What would happen if there was a mistake made during DNA replication 2. Are there any genetic diseases that can hinder DNA replication? 3. What is the frequency of DNA replication?
In response to your first question, if mistakes are made during replication they are often corrected before any damage is done. However, if a mistake is not corrected when it initially occurs, then the next DNA molecule that is replicated will have that mistake but think that it is the correct sequence.
In response to your second question, there aren't many diseases that are listed out that really hinder the process of replication, but there are other factors that do, such as many examples. This source holds a lot of examples, https://www.sciencedirect.com/science/article/pii/S0014482714004352
To answer your second question, I found a website that talks about inherited mitochondrial diseases that can hinder DNA replication. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2271032/
1. Is it possible for a DNA sequence to have the same number percentage of base pairings as another species? 2. How exactly does heat denature DNA? 3. Is it possible for the sequence to break? As in make a mistake in structuring or shape? If that even makes sense.
For your second question, because DNA is connected by both hydrogen bonds and covalent bonds, when heated enough, the hydrogen bonds will weaken to the point of separation. When this happens, the DNA gets unwinded and becomes single stranded. https://en.wikibooks.org/wiki/Structural_Biochemistry/Nucleic_Acid/DNA/DNA_Denaturation#:~:text=When%20a%20DNA%20solution%20is,together%20weaken%20and%20finally%20break.&text=The%20temperature%20at%20which%20the,the%20melting%20temperature(Tm).
To answer your third question, it is possible for a DNA sequence to break. When the body goes through metabolic changes, such as "reactive oxygen species", the DNA is damaged. DNA can also be damaged through external environment exposure to irradiation, ultraviolet light, and certain chemical agents. However, DNA can be recovered because organisms have checkpoint mechanisms. The cell will then go through a system to repair the damaged sequence. https://www.nature.com/scitable/topicpage/repairing-double-strand-dna-breaks-14432332/
In response to the first question, since percentages are purely based on sample size, it is possible for one species to have the same percentage of types of base pairings as another. If we are talking pure numbers, however, it is very unlikely.
To reply to your second question... i found a website that talks about heat denaturation and how it works. Specifically how heat causes hydrogen bonds to weaken which makes it easier to pull the two strands of DNA apart. http://www.umich.edu/~caparray/educ/dnapr/pg2.html
In regards to your first question, histones are proteins that associate with DNA in the nucleus and help it form into chromatin. For more information, the source i used was https://www.nature.com/scitable/definition/histones-57/#:~:text=Histones%20are%20a%20family%20of,in%20the%20formation%20of%20chromosomes.
1. Is there a difference between Gyrase and Topiosomerase? 2. How does the SSB Proteins prevent the DNA from reforming? 3. How does DNA ligase connect the Okazaki fragments?
To answer your first question, the difference between gyrase and topoisomerase is gyrase is involved primarily in supporting chain elongation during replication of the chromosome, whereas topoisomerase separates the linked daughter chromosomes. Source: https://www.sciencedirect.com/science/article/abs/pii/S0167478198001262#:~:text=DNA%20gyrase%20and%20topoisomerase%20IV%20are%20the,II%20topoisomerases%20present%20in%20bacteria.&text=Gyrase%20is%20involved%20primarily%20in,terminal%20stage%20of%20DNA%20replication.
To answer your question, SSB proteins prevent DNA from reforming by binding to the single strand of DNA through hydrogen bonds, removing the strands' need to reform. Source: https://proteopedia.org/wiki/index.php/Single_stranded_binding_protein
To answer your third question, DNA ligase connects the Okazaki fragments by forming a bond between the phosphate group of one strand and the deoxyribose group on another. Source: https://di.uq.edu.au/community-and-alumni/sparq-ed/sparq-ed-services/dna-ligation#:~:text=DNA%20ligase%20is%20an%20enzyme,lagging%20strand%20during%20DNA%20replication.
Hey Celeste! When I was researching your second question, I found that we will get more into this in 7.2 :) However, a brief summary would be that nucleosomes only make certain parts of the DNA accessible. The DNA that are wrapped too tightly are inaccessible for transcription and these genes are turned off. This shows that nucleosomes aid in the process of gene expression, because otherwise no genes would be turned off and every part of DNA would be transcribed and turned into proteins that aren't needed. I got this information from a different IB Bio website: ites.google.com/a/aisr.org/mun-ib/biology/topic-7-nucleic-acids/topic-7-2-transcription-and-gene expression#:~:text=Nucleosomes%20help%20regulate%20transcription%20because,the%20DNA%20would%20be%20expressed. I hope this helped!
To answer your third question, I used part of a really great video! (https://youtu.be/E9OIZo_H9Ug) The time slot is going to be from around 31:25 to 35:42. It explains how tandem repeats can be found in areas of the genome called polymorphisms, which account for the 1% of DNA that is unique to each individual. The highly repetitive sequences called tandem repeats are cut out from these areas and put through gel electrophoresis, where bands form based on the length of the sections (which is determined by the amount of tandem repeats in each individual). Because these are unique to each person, the bands can be analyzed against the DNA from a scene during DNA profiling.
1) What is the difference between x-ray diffraction and crystallography? I don't fully understand how they work. 2) Was a majority of Watson and Cricks process to get to the end model trial and error? Do we know how many test models they had created? 3) We may have discussed this and I forgot, is there a reason cytosine and guanine have 3 hydrogen bonds whereas adenine and thymine have 2?
to answer your 3rd question... I found a website that talks about why guanine and cytosine have three hydrogen bonds, compared to thymine and adenine which have 2. It mentions how having three hydrogen bonds creates a stronger connection between the two bases, and it also talks about how scientists can use this to figure out denaturation in DNA molecules. https://teaching.ncl.ac.uk/bms/wiki/index.php/Hydrogen_bonds#:~:text=Guanine%20pairs%20with%20cytosine%20with,bonded%20base%20pairs%20in%20DNA.
X-Ray Crystallography is used for identifying the atomic and molecular structure of a crystal. The atoms cause a beam of X-rays to diffract into a lot of different but specific directions. Crystallographers measure the angles and the intensity of the diffracted beams and can create a 3D picture of the electrons in the crystal.
X-Ray Crystallography uses the uniformity of light diffraction of crystals to find the structure of a molecule or atom. They use an X-ray to “hit” a crystallized molecule. The surrounding electrons will diffract when hit by the X-ray. This'll form a pattern called the X-ray diffraction pattern. This X-ray diffraction pattern is formed when X-rays are focused on a crystalline material, like a protein. Below is an extra resource describing in detail each process, I hope this helps!
1) Why is RNA primer used to initiate DNA polymerase? Why RNA? 2) What are other proven important roles of repetitive sequences in DNA, besides their protective function in telomeres? 3) Does anyone have any tricks or resources for remembering everything that has to do with 3 prime and 5 prime? I find this to be the hardest part for me to conceptualize!
Question 1- DNA Polymerase requires a primer to begin replication. It is not advanced enough to start on it's own. I don't have an exact answer about why the primer is RNA. I believe it's because it is only needed temporarily. It is a quick fix so that replication can begin. I was doing a little research and found that there can be DNA primers in certain organisms but our cells don't have or utilize those. I think these primers are especially important when it comes to the lagging strand. When you use RNA it isn't permanent. Since it's broken up the cell needs to go back and fill in and fix the strand, this is easier to do when you have a placeholder to switch with a permanent solution. Maybe that makes no sense but those are just the thoughts that ran through my head haha. https://www.sciencedirect.com/topics/medicine-and-dentistry/primer-rna
To help with question 3, I do not necessarily have any ways of memorization of my own but here are some links that could provide contexts for memorization.
1. Can the addition of a wrong nucleotide (say adding adenine to guanine) cause a genetic mutation/is it possible? 2. How long does it take for a lagging strand to replicate in comparison to the leading strand? 3. Does anybody know any fun acronyms to remember the order of each enzyme that is used in DNA replication?
To answer your first question, I found an article that talks just about this! I didn't think this was possible, but turns out these do cause genetic mutations that are actually pretty common. Apparently, Guanine-Thymine mutations are the most common in human DNA. At first the connected pair would stick out because they don't fit together, but then nucleotides would change shape in order to appear normal in the gene sequence and avoid correction by DNA polymerase. It's super interesting! Link: https://news.osu.edu/study-reveals-how-the-most-common-dna-mutation-happens/
To help answer your 2nd question, prokaryotic specifically bacterium E.coli can replicate at a rate of 1,000 nucleotide per second. IN eukaryotic, the speed of replication is 50 nucleotide per second. Although the leading strand continuously synthesizes and the lagging strand synthesizes in fragments, the process of replication happens relatively fast.
Question 1- DNA Polymerase requires a primer to begin replication. It is not advanced enough to start on it's own. I don't have an exact answer about why the primer is RNA. I believe it's because it is only needed temporarily. It is a quick fix so that replication can begin. I was doing a little research and found that there can be DNA primers in certain organisms but our cells don't have or utilize those. I think these primers are especially important when it comes to the lagging strand. When you use RNA it isn't permanent. Since it's broken up the cell needs to go back and fill in and fix the strand, this is easier to do when you have a placeholder to switch with a permanent solution. Maybe that makes no sense but those are just the thoughts that ran through my head haha. https://www.sciencedirect.com/topics/medicine-and-dentistry/primer-rna
To answer your first question, I found an article that talks just about this! I didn't think this was possible, but turns out these do cause genetic mutations that are actually pretty common. Apparently, Guanine-Thymine mutations are the most common in human DNA. At first the connected pair would stick out because they don't fit together, but then nucleotides would change shape in order to appear normal in the gene sequence and avoid correction by DNA polymerase. It's super interesting! Link: https://news.osu.edu/study-reveals-how-the-most-common-dna-mutation-happens/
1. What would happen if the bases A-T and C-G were to be created in uneven amounts? (Ex. Substantially more guanine produced than cytosine) 2. How small a molocule can X-Ray diffraction/crystallography observe and work with? 3. What can scientists use the 3D models that come from X-Ray diffraction/crystallography for?
To answer your 3rd question, Scientist can use 3D models from X-ray crystallography to state the difference between the arrangement of atoms and determine the function of biological molecules. Hope this helped!
In response to your second question, scientists can work with molecules with as few as 100 atoms, to do this requires the use of small-molecule crystallography. They can also see, in general, individual atoms. Here is a link that goes into more detail. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/x-ray-crystallography
For your first question, I couldn’t find anything specifically on what happens if they are in unequal amounts but I did find this source on how they are created and used. I hope this helps! https://www.khanacademy.org/science/high-school-biology/hs-molecular-genetics/hs-discovery-and-structure-of-dna/a/hs-dna-structure-and-replication-review
1. Is there any specific prokaryote or eukaryote that takes longer to replicate? (typical it would take 1,000 - 50 nucleotide per second) 2. If there are inconsistency with the base pairings (ex) unequal ratio, missing a purine or pyrimidine, etc.), what would be the health concerns be? 3 how do nucleosomes super coil and the process as to how it protects DNA?
For your third question, this website goes into detail about how nucleosomes help supercoil DNA and help to protect the genetic information, I hope it helps! https://ib.bioninja.com.au/higher-level/topic-7-nucleic-acids/71-dna-structure-and-replic/nucleosomes.html
1 - How, in detailed, does helicase work to uncoil and separate the DNA strands? 2 - Is there a trick anyone knows for how to remember all the enzymes involved in DNA replication? 3 - Since it is always happening, how many mistakes are made during DNA replication on average?
1. What would happen if a histone was damaged? How would that affect the DNA?
ReplyDelete2. Is the same DNA polymerase used for the whole strand of DNA? or do different polymerases switch off?
3. Are there different types of nucleosomes?
To answer your third question, I can find no mention of more than one type of nucleosomes. This doesn't mean that they don't exist, but it is likely that they don't exist.
DeleteTo answer your second question, On the leading strand the same DNA Polymerase is used throughout the replication process and the lagging strand as it takes place at the replication fork.
DeleteFor your first question, from what I can find histone damage is either uncommon or not researched as I couldn't find anything specific to that. If a histone was damaged, whatever force caused it would likely damage the cell as a whole. I could find information on decreased histone production, which leads to increased risk of genetic damage and increased transcription rates. It was observed that areas that usually have high nucleosome density stayed the same, while areas with low nucleosome density decreased, most likely because those genes were in some way not as valuable as those which were more highly protected. https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001098#:~:text=Cells%20that%20lack%20proteins%20required,genetic%20damage%20and%20early%20death.
Delete1. Do the lagging and leading strands finish at the same time?
ReplyDelete2. What is the purpose of nucleosomes?
3. What are other functions of non-coding DNA?
To answer your question, They finish at the exact same time as the lagging strand moves much quicker during replication.
DeleteCitation
https://www.nature.com/articles/nrm2828
For your second question, the purpose of nucleosomes is to aid in the process of supercoiling. DNA strands wrap around histones, creating nucleosomes, which are a core of 8 total histones, 4 pairs of the same. Nucleosomes are soiled into supercoils, which are them coiled into chromosomes. (Textbook)
DeleteTo answer your third question, non-coding DNA acts as a regulatory system for when and where genes should be turned on or off.
Deletehttps://medlineplus.gov/genetics/understanding/basics/noncodingdna/
For your first question I found from Oregon state that the lagging strand is looped out in such a way that it can be made at the same time as the leading strand.
Deletehttp://oregonstate.edu/instruction/bi314/fall11/dnarep.html#:~:text=How%20can%20both%20leading%20and,direction%20of%20leading%20strand%20synthesis%3F&text=The%20lagging%20strand%20is%20looped,time%20as%20the%20leading%20strand.
How many steps are there is supercoiling?
ReplyDeleteIs the leading strands replication faster than the lagging strand or do they end up at the same speed?
Where did the name Okazaki fragments come from?
To answer your third question, they were named after a Husband and Wife scientist pairing by the names of Reji Okazaki and Tsuneko Okazaki.
DeleteTo answer, your second question, the leading strand does go faster than the lagging strand because the lagging strand has to repeatedly go back and forth, whereas, the leading strand goes forward.
DeleteFor your third question, I found that Okazaki was the man who discovered the way in which the lagging strand of DNA is replicated in fragments, therefore they are named Okazaki fragments.
DeleteTo supplement the answers for your third question here is an article about Reji Okazaki and Tsuneko Okazaki and their discovery of Okazaki fragments:
Deletehttps://thebumblingbiochemist.com/365-days-of-science/tsuneko-okazaki-and-the-discovery-of-okazaki-fragments-also-what-those-are/
For your 1st question here is a BioNinja page about supercoiling:
Deletehttps://ib.bioninja.com.au/higher-level/topic-7-nucleic-acids/71-dna-structure-and-replic/supercoiling.html
1. How were Okazaki Fragments discovered?
ReplyDelete2. Why did DNA replication evolve in the 3' to 5' manner?
3. What are some ways that Histone could have evolved?
To answer your first question, Okazaki took E. coli and treated them with alkali to separate the hydrogen bonds. After sucrose density gradient centrifugation, the DNA was separated by weight and identified by a radiation test. This proved the concept of a lagging strand because the okazaki fragments were found at the top and the whole DNA was found at the bottom. As time went on the DNA at the top disappeared and the DNA at the bottom grew in quantity. This means that the Okazaki fragments were bonding, meaning that that is how the lagging strand replicates, in fragments.
DeleteIn response to your second question, the reason that DNA replication evolved as 3 prime to 5 prime is largely due to the proof reading of the created strand. If DNA replicated 5 prime to 3 prime there would be a problem when a misplaced nucleotide was taken out. Once that nucleotide was taken out there would be no way for a replacement to be put in the empty area as no high-energy bond will be broken to provide energy for polymerization. SO, the biggest reason that DNA replication evolved in the 3 prime to 5 prime manner is due to the amount of energy needed for DNA replication from 3 prime to 5 prime being much lower than from 5 prime to 3 prime.
Deletehttps://www.quora.com/Why-is-DNA-replicated-in-the-5-3-direction#:~:text=In%20the%205'%20to%203,as%20a%20good%20leaving%20group.
1) What are supernatants?
ReplyDelete2) When diffraction occurs, is there a certain or similar pattern they could fall into or is the way it scatters so there is no similarity, this being without using crystals?
3) What are proteins similar to histones?
To answer your first question, supernatants is the soluble liquid reaction after being centrifuged.
DeleteCitation: https://www.genscript.com/molecular-biology-glossary/11520/Supernatant
To answer your third question, nonhistone proteins that have the function of scaffolding the DNA are similar to histones.
DeleteCitation:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4889822/
To answer your first question, I found that the definition of supernatants is a volume of supernatants liquid!
DeleteTo supplement the answers for your 1st question here is a definition from the Oxford Dictionary:
Deletehttps://www.oxfordreference.com/view/10.1093/oi/authority.20110803100543158
1. Does using a blender to separate the phage from the bacteria always work?
ReplyDelete2. Is it possible for there to be an error in the DNA where the Cytosine doesn't pain up with Guanine?
3. Continuing off from question 2, what are the effects of this error if the cell doesn't take notice of it?
For your second question, this is possible and is the main reason errors occur, due to a process called tautomerization, which causes electrons to rearrange and allow for incorrect base pairings. https://www.sparknotes.com/biology/molecular/dnareplicationandrepair/section3/#:~:text=Errors%20in%20DNA%20replication%20can,by%20a%20process%20called%20tautomerization.
DeleteIn response to question 3, if the mismatched base pair is not noticed by any error correcting component, it becomes a permanent mutation within the cell that carries over to the offspring, thus the effects depend on the type of gene encoded by the mutation.
Deletehttps://www.nature.com/scitable/topicpage/dna-replication-and-causes-of-mutation-409/
Question 1- I tried to find information on other ways to separate the two and if the blender didn't always work but couldn't find much. Most of it was about cultures such as with yeast production being infected and being sure all the phage was gone. I think the blender should always work, I don't think the phage is strong enough to hold onto the bacteria or pellet.
Delete1. What exactly is topoisomerase?
ReplyDelete2. Why doesn't the end of a chromosome get copied sometimes?
3. How many types of DNA polymerase is there?
Question 1- Topoisomerase is an enzyme that binds to DNA and cuts the phosphate backbone of one or both strands. https://www.sciencedirect.com/topics/neuroscience/topoisomerase
DeleteQuestion 3- There are three kinds of DNA polymerase, they are called DNA polymerase I, II, and III. Here's a short website that defines the function of each one! https://teaching.ncl.ac.uk/bms/wiki/index.php/DNA_polymerase
DeleteQuestion 2- Sometimes a chromosome doesn't get copied because there is a small stretch of DNA that doesn't get covered by Okazaki fragments. I'm including this link to a Khan Academy lesson that will probably explain it much better than I can :) https://www.khanacademy.org/science/biology/dna-as-the-genetic-material/dna-replication/a/telomeres-telomerase
Delete1) What is the function of heterochromatin?
ReplyDelete2) What is the function of telomeres?
3) What would happen if DNA ligase didn't exist? How would the Okasaki fragments be affected?
In response to your second question, the function of telomeres is to prevent genes from being deleted at the end of a chomosome. This is due to the fact that enzymes like DNA polymerase cannot copy DNA all the way to the end of the strand and must stop early. If there were no telomeres then the genes would slowly be destroyed with every replication, instead the repeating codes of telomeres are cut off and do not efect any genes.
DeleteAllot, Andrew, and David Mindroff. Biology. Oxford University Press, 2014, p. 351.
In response to question 3, if DNA Ligase didn't exist in a cell, the Okazaki fragments would be unable to connect together, and the DNA molecule would remain incomplete, nullifying it's job within the cell.
Delete1. Is there an enzyme that brings nucleotides to DNA polymerase to use in replicating DNA?
ReplyDelete2. Are there examples of organisms running out telomeres? If so, what happened to them?
3. What is the difference between DNA topoisomerase and gyrase?
In regards to your second question, an enzyme called primase aids dna polymerase with replication. Primase makes an RNA primer, or short stretch of nucleic acid complementary to the template, that provides a 3' end for DNA polymerase to work on. For more in depth information, the source i used was https://www.khanacademy.org/science/ap-biology/gene-expression-and-regulation/replication/a/molecular-mechanism-of-dna-replication#:~:text=Primers%20and%20primase,of%20an%20existing%20DNA%20strand.&text=The%20problem%20is%20solved%20with,DNA%20polymerase%20to%20work%20on.
DeleteQuestion 1- the nucleotides are "free" and are within the cytoplasm. These free nucleotides actually come from old mRNA that has been broken down.
DeleteI could not find any information on any sort of additional enzyme or protein used to bring the nucleotides to the DNA polymerase. I believe they are just free floating and accessible to use as needed.
https://mi01000971.schoolwires.net/cms/lib/MI01000971/Centricity/Domain/519/transcription%20pogil%20answers.pdf
In response to your first question, I do not believe that there is a specified enzyme that brings nucleotides to DNA polymerase; DNA polymerase, being an enzyme itself, may just obtain the nucleotides themselves. I apologize, I was unable to find much on this subject. Below is an extra source on DNA polymerase specifically, hope this helps!
DeleteSource :)
https://scienceprimer.com/dna-polymerase#:~:text=DNA%20polymerases%20are%20the%20enzymes,of%20a%20strand%20of%20DNA.&text=In%20the%20polymerase%20chain%20reaction,by%20attaching%20short%20DNA%20primers.
1. What would happen if there was a mistake made during DNA replication
ReplyDelete2. Are there any genetic diseases that can hinder DNA replication?
3. What is the frequency of DNA replication?
In response to your first question, if mistakes are made during replication they are often corrected before any damage is done. However, if a mistake is not corrected when it initially occurs, then the next DNA molecule that is replicated will have that mistake but think that it is the correct sequence.
Deletehttps://www.nature.com/scitable/topicpage/dna-replication-and-causes-of-mutation-409/#:~:text=When%20Replication%20Errors%20Become%20Mutations,longer%20recognizes%20them%20as%20errors.
In response to your second question, there aren't many diseases that are listed out that really hinder the process of replication, but there are other factors that do, such as many examples. This source holds a lot of examples, https://www.sciencedirect.com/science/article/pii/S0014482714004352
DeleteTo answer your second question, I found a website that talks about inherited mitochondrial diseases that can hinder DNA replication.
Deletehttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2271032/
1. Is it possible for a DNA sequence to have the same number percentage of base pairings as another species?
ReplyDelete2. How exactly does heat denature DNA?
3. Is it possible for the sequence to break? As in make a mistake in structuring or shape? If that even makes sense.
For your second question, because DNA is connected by both hydrogen bonds and covalent bonds, when heated enough, the hydrogen bonds will weaken to the point of separation. When this happens, the DNA gets unwinded and becomes single stranded. https://en.wikibooks.org/wiki/Structural_Biochemistry/Nucleic_Acid/DNA/DNA_Denaturation#:~:text=When%20a%20DNA%20solution%20is,together%20weaken%20and%20finally%20break.&text=The%20temperature%20at%20which%20the,the%20melting%20temperature(Tm).
DeleteTo answer your third question, it is possible for a DNA sequence to break. When the body goes through metabolic changes, such as "reactive oxygen species", the DNA is damaged. DNA can also be damaged through external environment exposure to irradiation, ultraviolet light, and certain chemical agents. However, DNA can be recovered because organisms have checkpoint mechanisms. The cell will then go through a system to repair the damaged sequence.
Deletehttps://www.nature.com/scitable/topicpage/repairing-double-strand-dna-breaks-14432332/
In response to the first question, since percentages are purely based on sample size, it is possible for one species to have the same percentage of types of base pairings as another. If we are talking pure numbers, however, it is very unlikely.
DeleteTo reply to your second question...
Deletei found a website that talks about heat denaturation and how it works. Specifically how heat causes hydrogen bonds to weaken which makes it easier to pull the two strands of DNA apart.
http://www.umich.edu/~caparray/educ/dnapr/pg2.html
In regards to your first question, histones are proteins that associate with DNA in the nucleus and help it form into chromatin. For more information, the source i used was https://www.nature.com/scitable/definition/histones-57/#:~:text=Histones%20are%20a%20family%20of,in%20the%20formation%20of%20chromosomes.
ReplyDelete1. Is there a difference between Gyrase and Topiosomerase?
ReplyDelete2. How does the SSB Proteins prevent the DNA from reforming?
3. How does DNA ligase connect the Okazaki fragments?
To answer your first question, the difference between gyrase and topoisomerase is gyrase is involved primarily in supporting chain elongation during replication of the chromosome, whereas topoisomerase separates the linked daughter chromosomes.
DeleteSource: https://www.sciencedirect.com/science/article/abs/pii/S0167478198001262#:~:text=DNA%20gyrase%20and%20topoisomerase%20IV%20are%20the,II%20topoisomerases%20present%20in%20bacteria.&text=Gyrase%20is%20involved%20primarily%20in,terminal%20stage%20of%20DNA%20replication.
To answer your question, SSB proteins prevent DNA from reforming by binding to the single strand of DNA through hydrogen bonds, removing the strands' need to reform.
DeleteSource: https://proteopedia.org/wiki/index.php/Single_stranded_binding_protein
To answer your third question, DNA ligase connects the Okazaki fragments by forming a bond between the phosphate group of one strand and the deoxyribose group on another.
DeleteSource: https://di.uq.edu.au/community-and-alumni/sparq-ed/sparq-ed-services/dna-ligation#:~:text=DNA%20ligase%20is%20an%20enzyme,lagging%20strand%20during%20DNA%20replication.
Hey Celeste! When I was researching your second question, I found that we will get more into this in 7.2 :) However, a brief summary would be that nucleosomes only make certain parts of the DNA accessible. The DNA that are wrapped too tightly are inaccessible for transcription and these genes are turned off. This shows that nucleosomes aid in the process of gene expression, because otherwise no genes would be turned off and every part of DNA would be transcribed and turned into proteins that aren't needed. I got this information from a different IB Bio website: ites.google.com/a/aisr.org/mun-ib/biology/topic-7-nucleic-acids/topic-7-2-transcription-and-gene expression#:~:text=Nucleosomes%20help%20regulate%20transcription%20because,the%20DNA%20would%20be%20expressed. I hope this helped!
ReplyDeleteTo answer your third question, I used part of a really great video! (https://youtu.be/E9OIZo_H9Ug) The time slot is going to be from around 31:25 to 35:42. It explains how tandem repeats can be found in areas of the genome called polymorphisms, which account for the 1% of DNA that is unique to each individual. The highly repetitive sequences called tandem repeats are cut out from these areas and put through gel electrophoresis, where bands form based on the length of the sections (which is determined by the amount of tandem repeats in each individual). Because these are unique to each person, the bands can be analyzed against the DNA from a scene during DNA profiling.
ReplyDelete1) What is the difference between x-ray diffraction and crystallography? I don't fully understand how they work.
ReplyDelete2) Was a majority of Watson and Cricks process to get to the end model trial and error? Do we know how many test models they had created?
3) We may have discussed this and I forgot, is there a reason cytosine and guanine have 3 hydrogen bonds whereas adenine and thymine have 2?
to answer your 3rd question...
DeleteI found a website that talks about why guanine and cytosine have three hydrogen bonds, compared to thymine and adenine which have 2. It mentions how having three hydrogen bonds creates a stronger connection between the two bases, and it also talks about how scientists can use this to figure out denaturation in DNA molecules.
https://teaching.ncl.ac.uk/bms/wiki/index.php/Hydrogen_bonds#:~:text=Guanine%20pairs%20with%20cytosine%20with,bonded%20base%20pairs%20in%20DNA.
To answer your first question,
DeleteX-Ray Crystallography is used for identifying the atomic and molecular structure of a crystal. The atoms cause a beam of X-rays to diffract into a lot of different but specific directions. Crystallographers measure the angles and the intensity of the diffracted beams and can create a 3D picture of the electrons in the crystal.
X-Ray Crystallography uses the uniformity of light diffraction of crystals to find the structure of a molecule or atom. They use an X-ray to “hit” a crystallized molecule. The surrounding electrons will diffract when hit by the X-ray. This'll form a pattern called the X-ray diffraction pattern. This X-ray diffraction pattern is formed when X-rays are focused on a crystalline material, like a protein. Below is an extra resource describing in detail each process, I hope this helps!
Source :)
https://www.slideshare.net/FaisalHussain23/x-ray-crystallography-and-x-ray-diffraction-94681907#:~:text=2.,diffract%20into%20many%20specific%20directions.&text=This%20forms%20a%20pattern%2C%20this,the%20X%2Dray%20diffraction%20pattern.
Quick edit, the second description was supposed to say X-Ray Diffraction and not X-Rau Crystallography, my bad!
Delete1) Why is RNA primer used to initiate DNA polymerase? Why RNA?
ReplyDelete2) What are other proven important roles of repetitive sequences in DNA, besides their protective function in telomeres?
3) Does anyone have any tricks or resources for remembering everything that has to do with 3 prime and 5 prime? I find this to be the hardest part for me to conceptualize!
Question 1- DNA Polymerase requires a primer to begin replication. It is not advanced enough to start on it's own. I don't have an exact answer about why the primer is RNA. I believe it's because it is only needed temporarily. It is a quick fix so that replication can begin. I was doing a little research and found that there can be DNA primers in certain organisms but our cells don't have or utilize those. I think these primers are especially important when it comes to the lagging strand. When you use RNA it isn't permanent. Since it's broken up the cell needs to go back and fill in and fix the strand, this is easier to do when you have a placeholder to switch with a permanent solution. Maybe that makes no sense but those are just the thoughts that ran through my head haha.
Deletehttps://www.sciencedirect.com/topics/medicine-and-dentistry/primer-rna
To help with question 3, I do not necessarily have any ways of memorization of my own but here are some links that could provide contexts for memorization.
Deletehttp://www.informatics.jax.org/glossary/_5_prime
http://www.informatics.jax.org/glossary/_3_prime
https://www.ncbi.nlm.nih.gov/Class/MLACourse/Modules/MolBioReview/basepair.html
1. Can the addition of a wrong nucleotide (say adding adenine to guanine) cause a genetic mutation/is it possible?
ReplyDelete2. How long does it take for a lagging strand to replicate in comparison to the leading strand?
3. Does anybody know any fun acronyms to remember the order of each enzyme that is used in DNA replication?
To answer your first question, I found an article that talks just about this! I didn't think this was possible, but turns out these do cause genetic mutations that are actually pretty common. Apparently, Guanine-Thymine mutations are the most common in human DNA. At first the connected pair would stick out because they don't fit together, but then nucleotides would change shape in order to appear normal in the gene sequence and avoid correction by DNA polymerase. It's super interesting! Link: https://news.osu.edu/study-reveals-how-the-most-common-dna-mutation-happens/
DeleteIn response to your third question, I've never heard of an acronym for the enzyme order but I made one and I hope it maybe helps a bit!
DeleteHelicase-Gyrase-Primase-DNA Polymerase-DNA Polymerase-Ligase
Halle Goes Pacing Down DNA Lane
Its definitely not the best but I tried haha
To help answer your 2nd question, prokaryotic specifically bacterium E.coli can replicate at a rate of 1,000 nucleotide per second. IN eukaryotic, the speed of replication is 50 nucleotide per second. Although the leading strand continuously synthesizes and the lagging strand synthesizes in fragments, the process of replication happens relatively fast.
Deletehttps://www.nature.com/scitable/topicpage/cells-can-replicate-their-dna-precisely-6524830/
Question 1- DNA Polymerase requires a primer to begin replication. It is not advanced enough to start on it's own. I don't have an exact answer about why the primer is RNA. I believe it's because it is only needed temporarily. It is a quick fix so that replication can begin. I was doing a little research and found that there can be DNA primers in certain organisms but our cells don't have or utilize those. I think these primers are especially important when it comes to the lagging strand. When you use RNA it isn't permanent. Since it's broken up the cell needs to go back and fill in and fix the strand, this is easier to do when you have a placeholder to switch with a permanent solution. Maybe that makes no sense but those are just the thoughts that ran through my head haha.
ReplyDeletehttps://www.sciencedirect.com/topics/medicine-and-dentistry/primer-rna
not sure how to delete, this was in response to Alyssa
DeleteTo answer your first question, I found an article that talks just about this! I didn't think this was possible, but turns out these do cause genetic mutations that are actually pretty common. Apparently, Guanine-Thymine mutations are the most common in human DNA. At first the connected pair would stick out because they don't fit together, but then nucleotides would change shape in order to appear normal in the gene sequence and avoid correction by DNA polymerase. It's super interesting! Link: https://news.osu.edu/study-reveals-how-the-most-common-dna-mutation-happens/
ReplyDelete1. What would happen if the bases A-T and C-G were to be created in uneven amounts? (Ex. Substantially more guanine produced than cytosine)
ReplyDelete2. How small a molocule can X-Ray diffraction/crystallography observe and work with?
3. What can scientists use the 3D models that come from X-Ray diffraction/crystallography for?
To answer your 3rd question, Scientist can use 3D models from X-ray crystallography to state the difference between the arrangement of atoms and determine the function of biological molecules. Hope this helped!
Deletehttps://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/x-ray-crystallography#:~:text=15.2.-,3%20X%2DRay%20Crystallography,be%20discovered%20by%20this%20method.
In response to your second question, scientists can work with molecules with as few as 100 atoms, to do this requires the use of small-molecule crystallography. They can also see, in general, individual atoms. Here is a link that goes into more detail. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/x-ray-crystallography
DeleteFor your first question, I couldn’t find anything specifically on what happens if they are in unequal amounts but I did find this source on how they are created and used. I hope this helps! https://www.khanacademy.org/science/high-school-biology/hs-molecular-genetics/hs-discovery-and-structure-of-dna/a/hs-dna-structure-and-replication-review
Delete1. Is there any specific prokaryote or eukaryote that takes longer to replicate? (typical it would take 1,000 - 50 nucleotide per second)
ReplyDelete2. If there are inconsistency with the base pairings (ex) unequal ratio, missing a purine or pyrimidine, etc.), what would be the health concerns be?
3 how do nucleosomes super coil and the process as to how it protects DNA?
For your third question, this website goes into detail about how nucleosomes help supercoil DNA and help to protect the genetic information, I hope it helps!
Deletehttps://ib.bioninja.com.au/higher-level/topic-7-nucleic-acids/71-dna-structure-and-replic/nucleosomes.html
1 - How, in detailed, does helicase work to uncoil and separate the DNA strands?
ReplyDelete2 - Is there a trick anyone knows for how to remember all the enzymes involved in DNA replication?
3 - Since it is always happening, how many mistakes are made during DNA replication on average?