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The graph of f is given. Draw the graphs of the following

Calculus: Early Transcendentals | 8th Edition | ISBN: 9781285741550 | Authors: James Stewart ISBN: 9781285741550 124

Solution for problem 10 Chapter 1

Calculus: Early Transcendentals | 8th Edition

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Calculus: Early Transcendentals | 8th Edition | ISBN: 9781285741550 | Authors: James Stewart

Calculus: Early Transcendentals | 8th Edition

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Problem 10

The graph of f is given. Draw the graphs of the following functions. (a) y fsx 2 8d (b) y 2fsxd (c) y 2 2 fsxd (d) y 1 2 fsxd 2 1 (e) y f 21 sxd (f) y f 21 sx 1 3d

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Cell Biology on April 18, 20, 22, 2016 (All images taken from Professor Hennessey’s slide—edited by ChiWai Fan) Summary of Mitosis and Meiosis Mitosis produces daughter cells with the same genotype as the mother cell No genetic segregation or independent assortment in mitosis Meiosis produces cells with different mixtures of maternal and paternal genes because of: Independent assortment Genetic recombination Independent assortment and recombination happen in meiosis, not mitosis The point Goal of Mitosis: Faithful division of DNA so the daughter cells are genetically identical to the mother cell. Keep it real, keep it diploid, and keep it 100%. Goal of Meiosis: Mix it up. Produce haploid gametes with different genetic contributions from maternal and paternal sources for further genetic mixing by sexual reproduction. When things go wrong Aneuploidy. Abnormal number of chromosomes Recombination and Independent Assortment are supposed to happen. Aneuploidy shouldn’t Aneuploidy is when things go wrong. Recombination and independent assortment shouldn’t cause aneuploidy Aneuploidy can result from either primary or secondary nondisjunction Mistake happens in different stage Nullisomy is missing chromosomes. This is usually fatal Too many or not enough chromosomes can be bad Trisomy 21 (Down’s syndrome): Karyotype of a human. What the paired, homologous chromosomes should look like Aneuploidy in a cancer cell Not all cancer cells look like this. The point is that it doesn’t look normal at all Translocations can cause chromosomes to mix, like in #6. The longer chromosome has parts of other chromosomes in it. Cell choices when DNA is altered by damage, mutation or mistakes: 1. Correct it. Arrest the cell cycle and clean up the mess before proceeding. 2. Evolve. Live with the change as a good mutation and as a selective advantage 3. Die (necrosis) because there is no choice: cells naturally die 4. Cell suicide (apoptosis): cell chooses to die before it gets mutated to the point of causing cancer 5. Cancer DNA Repair DNA damage and replication mistakes and happen. What to do about it Repair the mistakes Some examples of DNA repair mechanisms: 1. Proofreading by DNA polymerase I 2. Nucleotide excision repair 3. Base excision repair 4. Double-strand break repair What happens if you can’t repair the mistake Either cell death, suicide (apoptosis) or the DNA mutations can be passed on during replication. A. Germ cell (sex cell) : Genetically inherited mutation B. Somatic cell: Cancer Nobel Prize in Chemistry for 2015 Tomas Lindahl: base excision repair Aziz Sancar: nucleotide excision repair Paul Modrich: mismatch repair A pyrimidine dimer that has formed within a DNA duplex following UV irradiation This is an example of the kind of DNA damage your skin gets in the sun This can also be caused by Ionizing radiation, common chemicals and thermal energy Luckily, our cells have a number of mechanisms to repair this kind of genetic damage Nucleotide excision repair after uv damage Nucleotide excision repair (NER) removes bulky lesions, such as thymine dimers and chemically altered nucleotides. 1. DNA damage is recognized by a protein complex 2. The helicase activity unwinds the DNA 3. It cuts it 4. It removes the damaged sequence 5. The gap is filled by a DNA polymerase 6. The DNA is rejoined by a ligase If all these worked to repair, you are very unlikely to get cancer At least 4 different gene products (enzymes) are necessary for this Xeroderma pigmentosum (XP) Xeroderma pigmentosum (XP) patients cannot repair sun-damaged DNA via Nucleotide Excision Repair (NER). Some help for XP patients may become available in the form of skin creams that contain DNA repair enzymes. If tumor suppressor genes or proto oncogenes are also affected, the result may be cancer. Patients with XP are at a high risk for developing skin cancers. Gene products (proteins) associated with XP: FYI Apoptosis: Programmed Cell Death and Cell Suicide Why have apoptosis Cell necrosis is ugly and messy. It generates all sorts of garbage Apoptosis is a neat and orderly way to kill cells How prevalent is it About 10 to 10 cells die each day in our bodies due to apoptosis Apoptosis and removal of the dead cell by a macrophage Apoptosis generates caspases which are specific proteases. Examples of the target proteins for these caspases are protein kinases, nuclear lamins and cytoskeletal proteins Caspases can be activated to cause apoptosis by either an extrinsic pathway (stimulated by receptors) or an intrinsic pathway Programmed cell death during development The paw of this mouse embryo is being sculpted by cell removal. The yellow dots are dying cells stained for apoptosis Cancer Oncogenes and tumor suppressors Oncogenes are positive regulatory factors which have mutated to become overactive For example, HER2 is a growth factor receptor. Overproduction causes more growth stimulation Tumor suppressors restrict growth. If mutated or inactivated, growth increases There are many kinds of cancer Cancer Treatment and the Cell Cycle If cell growth is out of control, just STOP IT. Then fix it and clean up the mess. Now you can resume. You stop everything (good and bad) Restriction point (checkpoint): some drugs such as Herceptin, inhibit growth factor simulation at the restriction point Radiation damages DNA and causes apoptosis at the S and G2 checkpoints Effects of DNA damage 1. DNA gets damaged by radiation, mutagens, etc. 2. BRCA enzymes help repair the damage. If they are mutated or missing, damage persists 3. A checkpoint should catch this damage and activate p53 4. p53 is a transcription factor that triggers either: p21 expression and cell cycle arrest or apoptosis If no p53 and no cell arrest, the cells proceed to either a tumor, cancer or death by necrosis p53 p53 (also known as protein 53 or tumor protein 53), is a tumor suppressor protein. It regulates the cell cycle and is involved in preventing cancers. P53 put cell cycle into arrest or tell cell to kill itself p53 has been described as "the guardian of the genome” because of its role in conserving stability by preventing genomic mutation. About 50% of human cancers have altered p53 p53 is a transcription factor that binds to DNA The 6 amino acids shown are the ones that are most often mutated in cancers Specificity for binding is based on amino acid R is arginine, it has a charge of +1 at pH=7.0 4/20/16 An example of a p53 effect Detect damage of DNAactivation of p53 (p53 only do things when it is phosphorylated) P53 is a transcription activator for p21. You only get p21 when DNA damage activates p53 which transcribes for p21. P21 now start cell cycle arrest.  What would happen if the p21 gene was mutated It does not cause cancer. It takes away cancer prevention.  What would happen if the damage can’t be fixed Apoptosis, if p53 and p21 worked but still can’t fix then apoptosis. If apoptosis don’t work, then may lead to cancer. In general, most cancers are due to loss of cell growth control because of mutations in: A. Oncogenes: They ignore inhibitory signals (like checkpoints). For example about 50% of human cancers have altered p53. B. Tumor suppressor genes. They don’t need stimulatory signals for cell division if mtuated p. 662. “Cancer is a genetic disease… but in most cases, it is not an inherited disease”. What does this mean  Cancer is usually due to somatic genetic mutations that are not heritable. (You may inherit a genetic predisposition for it though.) Some ways that contribute to triggering cancer: 1. Mutate BRCA enzymes. DNA damage not repaired properly 2. Mutate p53. Less expression of p21 and loss of checkpoint control 3. Mutation in p21. Inability to respond to p53 and loss of checkpoint control  BRCA, p53 and p21 are tumor suppressor genes  Note: Mutations can be either inherited or new. Mutation can either increase or decrease activities There are lots of different kinds of mutation. In general, cancer cells have problems with (all of these things): 1. Growth signals: A. Ignore inhibitory growth signals (tumor suppressors). B. Continue to grow in the absence of growth factors (oncogenes). 2. Defects in mitotic checkpoint proteins 3. Eliciting an apoptotic response Many cancers require multiple mutations in the same cell line  Would a RAS gene mutation always cause cancer Not always.  Many mutations might cause problem. Probability of cancer might increase if you have defected cell already plus mutation. Clonal growth of a cancer cell Tumor growth often requires many somatic mutations in cells from a common origin All of these cells came from mitosis of the first cell in this line. Are they all genetically identical Very low possibility to mutate an already-mutated cell. Mutation upon mutation is rare. Properties of cancer cells:  Cancer cells are immortalized  Cancer cells do not form differentiated tissues  Cancer cells are not under contact inhibition  Cancer cells are invasive (takes up other body part’s growing space; ex. huge liver)  Cancer cells escape apoptosis An immortalized cell line Stem cells can differentiate, Cancer cells don’t, (cancer cells stay as cancer cells) Cancer cells are immortalized, just like stem cells, but without control HeLa cells, still growing Most normal cells stop proliferating under contact inhibition Loss of contact inhibition: cancer cells spread nonstop Molecular changes required for metastasis: Cells need to lose cell-cell adhesion contacts Cells need to penetrate through the matrix (Extracellular matrix help prevent cancer cell metastasis) Loss of Cadherins is detected in all tumors Metastasis A benign tumor is a mass of cells (tumor) that lacks the ability to invade neighboring tissue or metastasize. It is not spreading into other tissues but still grows. It is continues to get bigger, it can turn into malignant. (It’s better to catch it before benign turn into malignant) A malignant tumor has metastasized and spread out to other tissues What causes cancer Cancer: accumulation of Mutations  Random mutations (mistakes at the assembly line)  Inherited mutations (pre-disposition)  Viral infections  Environmental factors (chemical; physical) First, something about mutations Mutations are heritable changes in the DNA sequence Genetic mutations are changes in the DNA sequence of genes (not all DNA carries genetic information) A gene is a locatable region of genomic sequence, corresponding to a unit of inheritance, which is associated with regulatory regions, transcribed regions, and/or other functional sequence regions Genotype: the DNA sequence Phenotype: the physical trait Codon usage table Why no Ts in this table Because it’s RNA. Codons are on Mrna Not all mutations cause changes in amino sequence. A point mutation changes only one of the nucleotides  Do all point mutations cause changes in amino acid sequences NO An example of the effects of point mutations 1. Since the mutant can’t make histidine, it can only grow if histidine is added, this is -mutant. 9 2. The rate of spontaneous mutations is about 1 in 10 nucleotides copied 3. If you screen enough of these bacteria, you can get a revertant that restores normal function  What’s the point of point mutations Point mutations can be either bad, good or do nothing  Are all mutations bad NO One way for a mitogen pathway to affect cancer Mitogen tells cell to start growing G1-Cdk and G1/S-Cdk are kinases that trigger progression into S-phase Activation of these kinases causes phosphorylation of a protein that keeps a transcription regulator inactivated (green thing is transcription regulator, it wants to tell the cell to grow; the red thing wrapped around green aka mitogen is trying to tell it to stay inactivated and do nothing) Genes get transcribed that produce proteins to stimulate cell division  What could happen if Rb was mutated and inactivated Now we don’t have transcription regulator. Now we have uncontrolled cell growth. So we hope checkpoints or apoptosis help the cell. If not due to many others having mutations too, then cancer.  If you have cancer that means many regions of the cell have problems. 4/22/16 Telomeres and Telomerase In many cells, the DNA gets shorter every time it is replicated. That may be one reason why we have long, untranscribed DNA (telomeres) at the ends. Telomeres are not transcipted, they don’t code for any information In stem cells, they have an enzyme called telomerase, which puts on telomeres. Stems cells would have a problem if each time they replicate, DNA get shorter because stem cells replicate a lot. The gene for telomerase is in all of our cells, but not all cells express telomerase. Telomerase makes sure you don’t lose DNA information when it shortens. Telomeres and cancer It is estimated that human telomeres can be up to 1kb long. They can lose about 100 base pairs from their telomeric DNA at each mitosis. This represents about 16 TTAGGG repeats. At this rate, after 125 mitotic divisions, the telomeres would be completely gone IN SOME CELLS. Telomeres shorten as you get older. When the telomeres are gone, there are problems with DNA replication and shortening of DNA strands. Cells deal with this by: o Ceasing to divide (replicative senescence) cells just stops dividing o Checkpoint arrest and DNA repair o Expressing telomerase to extend telomere length (cancer express telomerase and extend telomere so they never stop dividing) o Apoptosis, cancer or cell death Telomerase isn’t expressed in most mature somatic cells. Telomerase continues to be expressed in: o Germ cells; sex cells o Stem cells; as a baby so they can replicate a lot o Some protozoans like Tetrahymena (immortal) o Cancer cells. Telomere elongation is often used as a diagnostic for cancer cells Telomerase Telomerase makes telomeres. It is an RNA-dependent DNA polymerase (it makes DNA from RNA) Telomerase was first discovered in 1985 in Tetrahymena Tetrahymena are immortal, they continue to divide as long as there is food available How does telomerase work Telomerase, also called terminal transferase, is a ribonucleoprotein that adds a species-dependent telomere repeat sequence to the 3' end of telomeres 1. Telomerase binds to the 3’ end of DNA 2. The RNA template on the telomerase aligns with the DNA 3. Reverse transcriptase uses the open RNA sequences as a template to extend the DNA strand What is the genetic information in cells The Griffith Experiment (1928*) 1. Two different strains of pneumococcus bacteria were used to infect mice with pueumonia. A. Rough strain. Doesn’t kill mice B. Smooth strain. Kills mice 2. Can the non-killer strain (rough) be converted into killers (smooth) by genetic transformation What Griffith already knew I. The phenotype is the observable properties of a cell or organism that are genetically controlled. A. Rough strains formed small, irregular colonies on nutrient plates that were easily recognizable. They are non-virulent (don’t kill mice). This is their phenotype. B. Smooth strains form indicative large, smooth colonies. Smooth strains of these bacteria are encapsulated and virulent (killers). This is a different phenotype. The capsule may prevent them from being killed by the mouse, allowing them to live and infect the mouse with pneumonia Hypothesis to be tested: The genotype of a cell is determined by its DNA. DNA contains the genetic information that is passed on from cell to cell during cell division. Genotype (DNA) determines phenotype. Griffith never answered his hypothesis Bacterial polysaccharide capsule Results of the Griffith Experiment 1. Smooth kills. These bacteria can live inside mice lungs because capsule protects bacteria and cause pneumonia to kill mice if there’s MANY bacteria replicated 2. Rough don’t kill. No pneumonia. Mice live. 3. Dead smooth strains don’t kill mice. To cause pneumonia, the bacteria must be alive so that the bacteria can replicate and cause the infection. They heated and killed Smooth so they can’t replicate thus didn’t kill mice. 4. Transformation of live Rough cells turns them into killers. Add dead smooth cells with something from rough, to turn them into smooth killers. What is the transformation factor in smooth cells that makes them killers But Griffith didn’t figure out the transformational factor. What we know now that Griffith didn’t know Bacterial Transformation with foreign DNA (This changes the genotype of a cell) Little piece of foreign DNA got into genome of recipient cell and starts to replicate and express the foreign gene. Summary so far: 1. Rough strain pneumococcus does not kill mice 2. Smooth strain pneumococcus does kill mice by causing pneumonia Hypothesis: The genotype of a cell is determined by its DNA. DNA contains the genetic information that is passed from cell to cell during cell division. Genotype determines phenotype. Question to be asked: Can the phenotype of the rough strain be transformed by exposure to an extract of smooth strain cells so that they become killers  Did Griffith know what the transformation factor was NO What was the Transformation factor 1. It is heat stabile (not heat labile). Heating kills the bacteria but it doesn’t inactivate the transformation factor. 2. It must be incorporated into living bacterial cells. It can’t kill by itself. 3. What is the transformation factor Is it protein, lipid, DNA, RNA or what How could you tell  Would you expect the purified transformation factor to be toxic No Avery experiments (1940) Test extracts of heat-killed smooth cells by treating them with either protease, RNAse or DNAse and injects it into mice with live rough cells A. Protease destroys proteins. Does it destroy the transformation factor B. RNAse destroys RNA (but not DNA). Does it destroy the transformation factor C. DNAse destroys DNA (but not RNA). Does it destroy the transformation factor  How can you tell if the transformation factor was destroyed The mice live after being injected with rough cells and an extract that was treated with something that destroyed the transformation factor. What Avery saw Took smooth bacterial, heat and filtered dead bodies and called that the extract and divided into 3 tubes. 1. Protease didn’t destroy transformation factor 2. RNAse didn’t destroy transformation factor 3. DNAse destroyed transformation factor so mice live. DNAse destroyed the transformation factor so it was DNA. Avery’s Conclusion. Not everyone buy it. Hershey-Chase Experiment (1952) Main Questions Asked: When a virus (phage) infects a bacterium and replicates, is the infecting agent DNA or protein Is DNA the genetic information that is passed from the infecting virus to all of the progeny (new phages) How some viruses can replicate: 1. Virus injects its DNA into a cell 2. Some of the viral DNA is replicated 3. Some of the viral DNA is transcribed 4. The transcribed RNA is translated into viral proteins 5. The viral proteins and viral DNA are assembled into new viruses and they are released. (We know its DNA, but they didn’t) Not all viruses work like this, but the ones used by Hershey-Chase do (circled) The type of viruses used by Hershey-Chase Metabolic Labeling (2 different kinds) This procedure uses radioactive precursors (building blocks) to see what is made from those building blocks 1. Protein Labeling 35  S is radioactive sulfur; to make the proteins radioactive  The amino acids methionine and cysteine contain sulfur  Most proteins contain these amino acids 35  Therefore, adding S to growing phages or cells will make virtually all of the newly synthesized proteins radioactive  DNA does not contain any sulfur, so this doesn’t label DNA 2. DNA labeling 32  P is radioactive phosphorous  All DNA contains phosphorous (RNA has plenty of phosphrous) 32  Therefore, adding P to growing phages or cells will make the entire newly synthesized DNA radioactive. What Hershey-Chase did 1. Make two kinds of phages (viruses) by metabolic labeling: 35 A. Grow viruses on S. Makes hot (radioactive) protein coat with cold (not radioactive) DNA. 32 B. Grow viruses on P. Makes hot (radioactive) DNA with cold protein 2. Make two different bacterial cultures: A. Infected with viruses that has Hot Proteins but Cold DNA B. Infected with viruses that has Hot DNA but Cold Protein 3. Check to see if the new viruses that were made in the bacterial hosts and released from them (progeny) are radioactive or not  What is passed on from the parent (infecting) viruses to the progeny Is it parental protein or parental DNA Parental DNA Hershey-Chase Experiment continued 1. Infect bacteria with viruses that have hot DNA but cold protein: progeny is hot 2. Check progeny for radioactivity. There is radioactive DNA in the progeny: so some was passed on 3. Therefore, parental DNA is passed from the infecting phages to the progeny What if you did it the other way, with hot protein and cold DNA Then you have to conclude protein. So What Hershey-Chase showed that DNA (not protein) is passed on as the genetic material for viruses. I’m left with a few questions: A. How did they know it wasn’t RNA B. What could you change in the experiment to see if it was RNA since P-32 cause both RNA and 32 DNA radioactive Add radioactive uridine (U) instead of P C. Viruses aren’t even cells. How do we know this is relevant to all cells

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Textbook: Calculus: Early Transcendentals
Edition: 8
Author: James Stewart
ISBN: 9781285741550

Since the solution to 10 from 1 chapter was answered, more than 259 students have viewed the full step-by-step answer. The full step-by-step solution to problem: 10 from chapter: 1 was answered by , our top Calculus solution expert on 11/10/17, 05:21PM. This full solution covers the following key subjects: fsxd, given, draw, functions, fsx. This expansive textbook survival guide covers 17 chapters, and 879 solutions. The answer to “The graph of f is given. Draw the graphs of the following functions. (a) y fsx 2 8d (b) y 2fsxd (c) y 2 2 fsxd (d) y 1 2 fsxd 2 1 (e) y f 21 sxd (f) y f 21 sx 1 3d” is broken down into a number of easy to follow steps, and 45 words. Calculus: Early Transcendentals was written by and is associated to the ISBN: 9781285741550. This textbook survival guide was created for the textbook: Calculus: Early Transcendentals, edition: 8.

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The graph of f is given. Draw the graphs of the following