Wednesday, May 27, 2020

DPBioY1 1.6 - Blog 2020

TOPIC 1.6 - DPBioY1


2 Marks - On Time - Due August 7th, 2020!

2 Marks - Your Questions

3 Marks - Your thoughtful responses to others
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7 Total Marks

Textbook Link - https://drive.google.com/file/d/0B5dgiSZpFkXza0RJVUF2SWotZUk/view?usp=sharing

Powerpoint Link - https://drive.google.com/file/d/1zRP-DwcGZUROb4Qg-T6iIdoASS-eYGAr/view?usp=sharing

Student Sheet Link - https://drive.google.com/file/d/1QQC6h3sdSksXET69Z9dUJ1pJseQqKzNK/view?usp=sharing

83 comments:

  1. 1. What causes the spindle fibers to start forming and the centrosomes to move towards opposite poles? I know that cyclins are what regulates when the cell moves to different stages of the cell cycle so does that apply to mitosis too?
    2. What are the purposes of histone proteins besides being wrapped in DNA? Why are they wrapped in DNA?
    3. Do cells still complete their function or purpose while undergoing mitosis?

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    1. To answer your second question, histones are wrapped in DNA so that they can help regulate chromatin (what makes up DNA) and gene expression. Without histones the DNA would not be able to fit within the cell and life would not be possible without much larger cells.
      Sources: https://www.creative-diagnostics.com/blog/index.php/what-are-histones/
      https://www.google.com/search?q=what+would+happen+without+histones&rlz=1CAQIMT_enUS808US809&oq=what+would+happen+without+histones&aqs=chrome..69i57.7381j0j7&sourceid=chrome&ie=UTF-8&safe=active&ssui=on

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    2. For your third question, once cells are specialized and have a specific function, they usually no longer go through mitosis, instead if they need to be replaced, stem cells divide to create a replacement for the specialized cells. Since a stem cells purpose is to create new cells, I suppose by dividing they are continuing to fulfill their purpose, Source: https://www.eurostemcell.org/system/files/documents/resources/Introducing_SCs_slides_Jan2012.pdf

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  2. 1. WHat is the purpose of looking at the increase of something if it is not the cause of the other thing? (looking at the cigarette and death graph)
    2. Why do people who quit smoking still have the high risk of cancer? Dont the toxins clear at some point?
    3. Is there any way to reverse the effects of smoking?

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    1. To answer your third question, yes the harmful effects of smoking can be reversed, but it takes time. For the risk of cancer to clear it has to have been 10 years for the amount of risk to return to normal and it will be 15 years for the risks of heart attack and stroke to return to normal levels.
      Source: https://www.healthline.com/health/what-happens-when-you-quit-smoking#15-years

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    2. In response to your second question, for some people who quit smoking the toxins do clear. However, the DNA methylation (the addition of methyl groupsto DNA) can increase former smokers' likelihood of getting cancer. DNA methylation causes errors in gene function and genome stability is former smokers that may go away with time depending on the age the person quits smoking.

      I found my information at these two websites.
      https://www.sciencedaily.com/releases/2008/11/081117103644.htm
      https://www.health.harvard.edu/newsletter_article/cigarettes-the-lung-cancer-risk-lingers

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    3. For your first question, it is not necessarily about if it caused it not what correlation it can have with it such as the smoking of cigarettes increases the chance of a premature death. It does not mean it necessarily caused it however it can show us that it may have negative health problems.

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    4. For your second question I found that former smokers reduce there chances of having lung cancer down to 40%. There is still a possibility of getting lung cancer because there could still be toxins from the cigarettes in your lungs.

      Here is the article I looked at:
      https://www.hopkinsmedicine.org/health/conditions-and-diseases/lung-cancer/former-smoker-whats-your-risk-for-lung-cancer

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    5. To answer your first question I found a website that explains research they did on people who got lung cancer many years after they quit smoking. It talks about how smoking is very detrimental to the body and can affect all parts of the body (especially the lungs), but how after people quit smoking there body parts do not function at best creating a higher risk of cancer. Even years after someone has quit doctors still recommend going to get screened because there is still risk of cancer.Smoking can also permanently damage certain bodily organs creating a higher risk of cancer.

      https://www.verywellhealth.com/risk-of-lung-cancer-in-former-smokers-3971884

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  3. 1. How exactly does the cell self-destruct during apoptosis?
    2. Can DNA mutations lead to benefits in cellular function, and if so what are they?
    3. Do malignant tumors do anything? Do they function and survive only for themselves or do they work with the surrounding tissues?

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    1. To answer your first question here is a quotes from a website I found on how cells perform in apoptosis. "During apoptosis, the cell shrinks and pulls away from its neighbors. Then the surface of the cell appears to boil, with fragments breaking away and escaping like bubbles from a pot of hot water. The DNA in the cell’s nucleus condenses and breaks into evenly sized fragments. Soon the nucleus itself disintegrates, followed by the entire cell. A cellular cleanup crew made of phagocytic cells — immune cells that engulf and dispose of dead cells and debris—arrives on the scene to mop up the remains" (website linked below if you want to read more into this)

      https://www.livescience.com/12949-cell-suicide-apoptosis-nih.html

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    2. In response to your second question, there are a few gene mutations that have improved cellular function. Some of those include sickle cell anemia that protects against malaria and lactose tolerance in societies that raised cows and goats.
      There is also trichromatic vision (seeing red, blue, and green) in primates unlike many other vertebrates.
      I found my information on these websites.
      https://sciencing.com/the-advantages-and-disadvantages-of-mutation-12578847.html
      https://www.frontiersin.org/articles/10.3389/fevo.2017.00034/full

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    3. For your third 3rd question, Some malignant tumors remain localized and encapsulated, at least for a time; an example is carcinoma in situ in the ovary or breast. Most, however, do not remain in their original site; instead, they invade surrounding tissues, get into the body’s circulatory system, and set up areas of proliferation away from the site of their original appearance. The spread of tumor cells and establishment of secondary areas of growth is called metastasis; most malignant cells eventually acquire the ability to metastasize. Thus the major characteristics that differentiate metastatic (or malignant) tumors from benign ones are their invasiveness and spread.
      https://www.ncbi.nlm.nih.gov/books/NBK21590/

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  4. 1. What are some different uses of finding the mitotic index?
    2. How do cells receive signals to let them know they need to go through mitosis to replace cells?
    3. What factors lead to apoptosis being ineffective in mutated cells?

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    1. To answer your first question, the mitotic index can be used to help predict the cancer cells response to chemotherapy. I found a website that talks more about this idea.

      https://www.philpoteducation.com/mod/book/view.php?id=779&chapterid=1123#/

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    2. In response to your second question, the reason apoptosis becomes ineffective in mutated cells is that the gene that triggers apoptosis (TP53) is the most frequently mutated gene. So, the first thing to go in most mutated cells is the ability to realize they have become malignant.
      I found my information at this website under Suppressing Pro-apoptotic Protein Expression.
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4091735/

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    3. To your 3rd question, Apoptosis is considered a vital component of various processes including normal cell turnover, proper development and functioning of the immune system, hormone-dependent atrophy, embryonic development and chemical-induced cell death. Inappropriate apoptosis (either too little or too much) is a factor in many human conditions including neurodegenerative diseases, ischemic damage, autoimmune disorders and many types of cancer. Although many of the key apoptotic proteins have been identified, the molecular mechanisms of action or inaction of these proteins remain to be elucidated.
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2117903/

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  5. 1. What breaks down the nuclear membrane in prophase? How does the cell deal with the leftover material from the membrane?
    2. How does a cell fix microtubules that are not properly attached? What are the effects of microtubules being attached incorrectly?
    3. What is the average time it takes for mitosis to occur (specifically prophase to telophase) and how does it vary between types of cells?

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    1. To answer your second question, from what I could find, if the microtubules are improperly attached, they just fix themselves. Microtubules have a test to see if they are strong enough and in the right spot, so if the microtubules are improperly attached the test will expose that. With that being the case, there are no effects of being attached incorrectly.
      Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2358929/

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    2. To answer your first question, in prophase the nuclear membrane is broken down by changes in its three components. There is not one specific thing that results in the break down of the nuclear membrane or envelope. The nuclear envelope is broken down when the nuclear membranes are parted into vesicles, when the nuclear pores dissociate, and when the nuclear lamina depolymerizes.
      More information about the break down the nuclear envelope can be found here: https://www.ncbi.nlm.nih.gov/books/NBK9890/#:~:text=The%20nucleus%20during%20mitosis.,the%20nuclear%20envelope%20breaks%20down.

      The left over material from the envelope is stored in fragments in vesicles. After the cell has divided, the vesicles reassemble around the two sets of chromosome.
      More information can be found here:
      https://www.nature.com/scitable/topicpage/mitosis-14046258/

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    3. For your third question, the average time it takes is roughly about 2 hours when it begins going through PMAT. It can differ based on the speed of the metabolism and the program for the individual cell like in human's liver cells it can take up to a year.
      citation https://www.sparknotes.com/biology/cellreproduction/cellcycle/section2/

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  6. For your 3rd question, The length of the cell cycle is important because it determines how quickly an organism can multiply. For single-celled organisms, this rate determines how quickly the organism can reproduce new, independent organisms. For higher-order species the length of the cell cycle determines how long it takes to replace damaged cells. The duration of the cell cycle varies from organism to organism and from cell to cell. Most of the differences in cell cycle duration between species and cells are found in the duration of specific cell cycle phases. DNA replication, for example, generally proceeds faster the simpler the organisms. One reason for this trend is simply that prokaryotes have smaller genomes and not as much DNA to be replicated. Across species and organismal complexity, embryonic cells have an increased need for rapidity in the cell cycle because they need to multiply for the development of the embryo.
    https://www.sparknotes.com/biology/cellreproduction/cellcycle/section2/

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  7. 1. Is it possible for a genetic mutation not lead to cancer, but instead something beneficial to the human body?
    2. How did the cell evolve in order to perform the function mitosis?
    3. Where did the process of mitosis come from?

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    1. To answer your third question, I couldn't find a lot of information about the origin of mitosis, but I did find that mitosis evolved from molecular machinery found in prokaryotes used for DNA replication.
      Source: https://en.wikipedia.org/wiki/Origin_and_function_of_meiosis#:~:text=If%20meiosis%20arose%20from%20prokaryotic,replication%20and%20segregation%2C%20and%20meiosis

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    2. For your second question, it most likely came about as they began absorbing and forming a symbiotic relationship with early mitochondria and during cell division would transfer the mitochondria equally. from their spindle fibers and centrioles developed as a natural response to the formation of the nucleus and that's how mitosis developed.
      Citation https://www.thoughtco.com/binary-fission-vs-mitosis-similarities-and-differences-4170307

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  8. To answer your first question, it is possible for a genetic mutation to not affect your health. Genetic mutations range from negatively affecting your health, like causing cancer, not affecting you at all, or being beneficial. Examples of beneficial genetic mutations can be found here: https://www.businessinsider.com/genetic-mutations-that-make-you-more-awesome-2016-1#cetp-and-the-low-cholesterol-mutation-6

    Source: https://ghr.nlm.nih.gov/primer/mutationsanddisorders/neutralmutations

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  9. 1) What specific chemical compounds inside of cigarettes make them harmful?
    2) Are there any other uses for actin and myosin?
    3) What are reasons that the mitotic index can fluctuate?

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    1. For your first question I found that there are many harmful ingredients in cigarettes. One of the most dangerous ingredients is nicotine which is an addictive drug that produces one of the most harmful chemicals in tobacco smoke. Another chemical inside cigarettes is hydrogen cyanide which is a poisonous and flammable liquid. There are many other chemicals inside of cigarettes that make them harmful but these two are the most harmful.

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    2. Here is the link I found this off of:
      https://www.cancer.org/cancer/cancer-causes/tobacco-and-cancer/carcinogens-found-in-tobacco-products.html

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    3. To answer your third question, the mitotic index can fluctuate if carcinogens are causing the cells to reproduce at a faster rate. If the cells are not reproducing at a normal rate there will be an obvious issue.
      https://en.wikipedia.org/wiki/Mitotic_index

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    4. To answer your second question, the actin and myosin are also used to make up the skeletal muscle. The actin and myosin are repeatedly formed by the myosin thick filaments being surrounded by the actin thin filaments. These being so compact make up a functioning portion of a muscle cell.
      I got my information here:
      https://study.com/academy/lesson/muscle-contraction-actin-and-myocin-bonding.html#:~:text=as%20rigor%20mortis.-,Lesson%20Summary,chains%20in%20the%20thin%20filament.

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  10. Unit 1.6 questions
    1. One average how long does the supercoiling of DNA take?
    2. How many cells are normally located inside a tissue?
    3. Are there any diseases or illnesses that can invade benign tumors and turn them into malignant tumors?
    4. How are the tubular structures formed in plant cells?

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    1. For your third question, though not caused by diseases (from what I can find), Benign tumors can become malignant through a process called tumor progression, caused by abnormal transcription within the tumor. This can be caused by aging, genetic factors, or environmental factors. More info: https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/tumor-progression#:~:text=Tumor%20progression%20is%20driven%20by,influence%20expression%20of%20the%20genome.

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    2. To answer your second question, National Geographics describes the concept of knowing exactly how many cells are in the human body as a very complex subject but they estimate that in the skin tissue as a whole there are around 35 billion cells.
      https://www.nationalgeographic.com/science/phenomena/2013/10/23/how-many-cells-are-in-your-body/#close

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    3. To help answer your fourth question, the vacuole being the largest organelle in the plant cell and aids in cell division. When the cell begins going through mitosis, the dynamic of the vacuole changes and forms tubular structures within the vacuole membrane. This link explains more about that by experimenting with tubular structures in tobacco cells: https://pubmed.ncbi.nlm.nih.gov/14581629/

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  11. 1) Does anyone know any easy ways to remember the cell cycle?
    2) What would happen if the cyclin proteins were to make a mistake and begin the cell cycle too early?
    3) What is the average time for a cell to go completely through the cell cycle?

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    1. To answer your third question, I found that for more complex mammals with quick-dividing cells (like human cells), the process normally takes around 24 hours. The more simple the cell structure, the less time the cell cycle takes. The websites I found have tons of information that I can't give justice, so here are the links if you are interested in more specific details regarding variation in the process and why:
      https://www.sparknotes.com/biology/cellreproduction/cellcycle/section2/#:~:text=Usually%2C%20cells%20will%20take%20between,only%20takes%20about%202%20hours.
      https://www.ncbi.nlm.nih.gov/books/NBK9876/#:~:text=The%20cell%20grows%20(more..,and%20M%20about%201%20hour.

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    2. To answer your first question, I've seen some people use the mnemonic of Italian People Make Awful Taco Crunch (interphase, prophase, metaphase, anaphase, telophase, cytokinesis) or there is People Meet And Talk which covers prophase, metaphase, anaphase, and telophase. There is also this great quizlet that someone made which can be very beneficial when studying the cell cycle: https://quizlet.com/8205922/tricks-to-remember-each-stage-of-cell-cycle-flash-cards/

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    3. In regards to your second question, if a cyclin were to ever malfunction in a way to start cell reproduction faster, it would cause the cell to become cancerous, as the cells it produces would have the same fast reproductive qualities.

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3016250/

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    4. If the cyclin proteins made a mistake and began the cell cycle to early nothing bad that would affect the body would happen. If the cyclin keeps on repeating the mistake then bad things will happen since it is turning the cell into a tumor.
      Info http://genesdev.cshlp.org/content/32/9-10/620.full#:~:text=Mistakes%20during%20mitosis%20lead%20to,of%20trisomy%2021%20in%20humans.

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  12. In response to your second question, I could not find specific information to how it could be harmful, but I found that there is a process of negative supercoiling which uncoils the supercoiling that has already taken place. This could negatively affect the processes inside of the cells.
    Hope this helped!
    Here is the link I used: http://earth.callutheran.edu/Academic_Programs/Departments/BioDev/omm/topo1/frames/coil.htm

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  13. 1) What do the G phases in the cell cycle do?
    2) Why do chromosomes separate at the sister chromatid in the v shape rather than just down the middle by the long chromatid shape? Does it have to do with the way the centromere attaches it after replication?
    3) How can chromosomes uncoil in telophase if they are so much longer than the diameter of the nucleus?
    4) Are the polls located at opposite ends of the whole cell, or opposite sides within the boundaries of the nuclear membrane before it broke down?

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    1. In response to question 1, there are two G phases in the cell cycle, G1 and G2, which each have different roles. The G1 phase (first gap phase) is when the cell begins to grow larger, copies the organelles, and starts to create molecular building blocks that will be needed later in the process. The G2 phase (second gap phase) happens after the S phase and before G1. In this phase the cell is still growing, proteins/organelles are being created, and the cell begins to reorganize its contents to prepare for mitosis and ends when it begins.
      https://www.khanacademy.org/science/biology/cellular-molecular-biology/mitosis/a/cell-cycle-phases

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    2. For your third question, When the chromosomes uncoil into chromatids, the DNA is still wrapped very tightly around itself, just not nearly as tightly as chromosomes, which fold onto themselves around 10,000 times. More info: https://www.nature.com/scitable/topicpage/dna-packaging-nucleosomes-and-chromatin-310/

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    3. For your fourth question, the poles are located at opposite ends of the whole cell. Here is the source I utilized: https://www.nature.com/scitable/topicpage/mitosis-14046258/#:~:text=Mitosis%20is%20the%20process%20in,cell%20into%20two%20daughter%20cells.&text=As%20they%20move%2C%20they%20pull,opposite%20poles%20of%20the%20cell.

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    4. In response to your second question, sister chromatids are utilized in chromosomes so that the DNA is much more compact that it would be within the nucleus as chromatins, and the reason they are split is because each pair has identical DNA to make both cells perform the same function at the same rate.

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  14. To answer your third question, active eukaryotic cells will all go through the cell cycle in order to grow and divide (since those are a couple of the 7 functions of life). However, some cells are not always dividing like others are. This is what the "exit" G0 is for. In this state, the cell can rest and function as it normally would without preparing for division. This is called terminal differentiation. Another definition of this term is: A cell sufficiently committed to a particular function that it can no longer divide(https://medicaldictionary.thefreedictionary.com/terminally+differentiated+cell) A cell can stay in G0 permanently, like in terminal differentiation, or it can return to the cell cycle once the proper triggers and signals are given.
    Another website used: https://teachmephysiology.com/basics/cell-growth-death/cell-cycle/

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  15. 1. What is the most important step in mitosis that would drastically change cell division if not present?
    2. Why is it that only mitochondria and chloroplast increase during interphase?
    3. Could someone explain and provide an example on how to find mitotic index, I am having trouble comprehending it?

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    1. For your third question, the mitotic index is the number of cells in mitosis/the total number of cells. Looking at an image through a microscope, it should be clear which cells are going through the stages of mitosis because they look different. I hope that helps!

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    2. The Mitochondria and chloroplast grow like this during interphase in order to prepare for mitosis again.
      I got my info from: http://www.brooklyn.cuny.edu/bc/ahp/LAD/C9/C9_interphase.html#:~:text=Stocks%20of%20energy%20are%20accumulated,major%20phase%20in%20the%20cycle.

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  16. 1. Something I don't understand is the way a majority of cell cycle diagrams are set drawn. Why is it that the G2 phase and mitosis tend to be at the top rather than G1? Why are the final stages at the top of the cycle?
    2. The lesson said the cell cycle is continuous. But cyclins can keep the cell from dividing, whether that's temporary or permanent. So, are cells constantly dividing otherwise? If that's true, do different cells take longer to complete a cycle than others to allow them to complete their tasks?
    3. There are things vital in mitosis but we don't talk about them otherwise. More specifically the MTOC and lamella. Where do they go when they have finished their job? Does the MTOC remain in the cell or does it dissolve and reform?

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    1. In regards to your first question, I wasn't able to find much information on why the diagrams are set up that way, but I was able to find different diagrams that are set up in a more traditional way. There is an image on https://biologydictionary.net/interphase/ under the heading "Stages of Interphase" that has mitosis at the center of the top and G1 directly following on the right side. I also have the diagram we drew in 9th grade bio that looks like this that I can send you! After looking through several images of the cell cycle, I noticed that the configuration can differ. Sometimes mitosis is at the top, the right side, at the bottom... I don't think it matters too much as long as you know what each step involves and what step follows :)

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    2. To answer your second question, cells don't continuously divide unless there are cells in the body that are missing or have died. If the cell does continuously divide for no reason, its most likely that the cell has a mutation in its DNA and can cause cancer.

      I found my info from: https://www.nature.com/scitable/topicpage/cell-division-and-cancer-14046590/#:~:text=Mutations%20in%20genes%20can%20cause,can%20develop%20into%20a%20tumor.

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    3. To answer your third question, the MTOC and lamella both perform other functions in bodies of cell other than in Mitosis, for instance, the MTOC is used to manage flagella and cilia as well as the spindle fibers, while lamella mainly appear in respiratory organs, therefore they would both most likely stay inside a cell after Mitosis.

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    4. MTOC is the "skeleton" of the cell. Just like in our bodies, this microskeleton allows for structure and movement. Thus, the skeleton is always present, but it gets built up and taken apart at different times based on the motion and structure that is required. I hope that helps. In 9th grade we learned about the MTOC as the cytoskeleton... built from microtubues and microfilaments. :) Hope that helps.

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  17. For your first question, contractile proteins are proteins that mediate sliding of contractile fibers of a cell's cytoskeleton, and of cardiac and skeletal muscle. Here is the source I utilized: https://www.nature.com/subjects/contractile-proteins

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  18. 1. Why do chromosomes supercoil in prophase when they take up the same amount of space as they would uncoiled?
    2. What would happen if the attachments in metaphase were to be incorrectly attached?
    3. How does the cell recognize that it has to stop interphase and enter mitosis?

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    1. For your second question I believe if anything were to go wrong or be attatched incorrectly then the cell would go into apoptosis to ensure that only healthy and functioning cells reproduce. Here is a website that goes into a bit more detail. https://www.livescience.com/12949-cell-suicide-apoptosis-nih.html

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    2. To answer your 1st question,chromosomes supercoil to compact themselves, not only to fit within their nuclei but also so that they are short and compact enough to be separated and moved to opposite ends of the cell

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    3. To answer your second question,it is the cyclins and oncogenes that aids and controls the cell cycle respectively. Slide 25 of the 1.6 power point goes into more detail

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    4. To adress your 3rd question, there is a horomonal trigger that tells the cell once it has completed G1 to continue on to S1 and so on and so forth. It is a cyclin dependent kinase, usually the horomon will activate the cyclin dependent kinase complex. This abstract goes into more detail on how the CDK complex works and how it relates to how the cell decides to go into mitosis after interphase. https://pubmed.ncbi.nlm.nih.gov/11719058/

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  19. 1. When seeing how many chromosome there are during anaphase, do you count the number of v shapes, or each end of the v shapes?
    2. Can someone help me find an easy way to find the mitotic index?
    3. Why do the centromeres and telomeres go to different sides of the nucleus?

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    1. To answer your first question, you would count the v shapes as those are the chromosomes and the ends of the v shapes are the telomeres

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    2. for question two if you mean how you wold find it for a set of cells you wold just count the amount of cells performing mitosis and divide that by the total cell count.

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  20. 1 - Are all viruses potential carcinogens or are there only specific viruses with that possibility?
    2 - About how long does the supercoiling of chromosomes process take?
    3 - Are all carcinomas malignant tumors, if so then why are they called carcinomas and malignant tumors, is it a situation where all carcinomas are malignant tumors but not all malignant tumors are carcinomas?

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    1. Question 2- Interphase lasts about 24 hours in animal cells from what I've read, and this is when the supercoiling process occurs. So I think its safe to say its anywhere from 1-24 hours, although, it's difficult to get a closer estimate.

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  21. 1. What specific chemicals are classified as carcinogens?
    2. What viruses cause mutations and how common are those viruses?
    3. Do all tumors become cancer and/or cancerous?

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    1. in response to your first question,carcinogens are classified by whether they are genotoxic or nongenotoxic. Genotoxins cause irreversible genetic damage or mutations by binding to DNA, and nongenotoxins don't directly affect DNA but promote growth in other ways. They can do this through organic compounds and hormones. Chemicals that perform these functions have the potential to be classified as carcinogens. This website has a little more information on carginogens, hope it helps! https://www.britannica.com/science/carcinogen

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    2. In response to question 3 no not all tumors become cancer some of the are benign meaning they do not spread.

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  22. 1. How can a chromosome shrink down so small? I get that it's technically through supercoiling and a chemical process, but i just dont get how its physically possible for something 50,000um long to just be compacted that much and simply not take up space.
    2. What would it do to the body/body's cells if the body's cells malfunctioned at the G1 stage and didnt complete it correctly?
    3. What has to happen in the cells for a benign tumor to become cancerous?

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    1. Question 2- if a cell has malfunctioned and the G1 stage has not been completed correctly it will not continue to S phase. There are many things the cell checks (cyclins keep this in check). If the cell is not ready to divide then it will go back and stay in a G0 stage (it basically just sits and rests)
      https://www.khanacademy.org/science/biology/cellular-molecular-biology/stem-cells-and-cancer/a/cell-cycle-checkpoints-article

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  23. To answer your first question I like to think of it as a string, when the string is fully laid out then it takes up a large amount of space, but if you coiled it, or honestly just crumpled it up it becomes more compact. Similarly when you pull a slinky it stretches and takes up more space, but when it’s in it’s condensed state then it takes up signifigantly less space. I hope these analogies helped, here is a website that detailes how the same object can take up two different amounts of space while still maintaining it’s same mass. https://www.ibm.com/support/knowledgecenter/en/ssw_ibm_i_73/cl/cprobj.htm

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  24. 1. what are some alternative cancer resentments?
    2. is it ever possible for nerve cells to reproduce?
    3. what is believed to be the most common cause for oncogenes to not function properly.

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    1. Question 2- From what I understand, nerve cells (AKA neurons) cannot reproduce, however, more can just be created instead.

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    2. Question 3- proto-oncogenes are what assist cell growth, when these are mutated or there are too many cell growth can become uncontrolled leading to tumors. https://www.cancer.org/cancer/cancer-causes/genetics/genes-and-cancer/oncogenes-tumor-suppressor-genes.html

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    3. #2, it used to be thought that nerve cells never reproduce. It has been discovered recently, however, that some nerve cells do reproduce. This is an example of what we used to know, that has been replaced with new information as we continue to do scientific research.

      Regarding "Unknowns" response to question #3, Protooncogenes control cell reproduction not growth. Be careful when you use the word growth as that means "getting bigger." Reproduction equals making more. This is a common mistake in answering DP type questions. Word choice is important.

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  25. 1)Are there any pathogens like viruses that could also be considered carcinogens?
    2)If cytokinesis always occurs after Mitosis, why do we consider it a separate stage of cell life?
    3)Can cancer occur within plant cells?

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    1. Question 3- I couldn't find very many sources about this, however, from what I understand plant cells can get cancer, but it can not travel easily throughout the plants because the cell wall prevents it from doing so. The cancer that plants get is different from cancers that animals get. A good example is when the plant experiences excessive and uncontrolled growth or when a tree forms knots.

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    2. Question 1- From my understanding,
      yes not only viruses can be considered carcinogens but other pathogens as well such as bacteria. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4276961/#__sec2title
      Types of pathogens in connection to cancer: https://www.immunopaedia.org.za/immunology/special-focus-area/2-cancer-tumours/pathogens-and-cancer/
      Bacteria:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1518971/

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    3. For your second question. Mitosis is defined as the division of the nucleus. Therefore cytokinesis, which is the separation of the cytoplasm and cell membrane, is a separate event. However, cytokinesis always follows the division of the nucleus. Hope that helps.

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  26. 1) Are there any uses for cyclin proteins other than to aid in cellular reproduction?
    2) Are there any situations in which the formula to determine the mitotic index is not reliable and other methods would need to be used?
    3) Is it possible for the DNA molecules to not supercoil properly and then lead to defects in the DNA?

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  27. 1 - Cyclins control "cycles." Thus their name when discovered in controlling the cell cycle. We do use cyclins in the lab to research cancer causes and treatments as cancer is the disruption of the cell cycle.

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  28. 1. When cells go through mitosis and in turn create more cells, do they take up more room and cause other cells to squish along one another?
    2. Was there anyone who discovered the idea of cylins before Tim Hunt?
    3. Do begnin cancer cells just float around the body with no purpose? Does the body identify them as cancer cells and get rid of them or do they go through mitosis and create more?

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DPBioY1 - 2020 - 2.9 & 8.3 Photosynthesis

DPBioY1 - 2020 - 2.9 & 8.3 Photosynthesis  2 marks for your questions 3 marks for your reply 2 marks for submitting on time