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Lecture 26 (From Protein to Gene: Translation) Pre-Lecture
Task 1: Pre-lecture Introduction –Video “Protein Synthesis: The Translation Process”
This video has two segments showing animations of the translation of mRNA into protein. The first segment gives you a good overview of the process and also includes the processing of a protein after it has been made. The second segment is more detailed in its portrayal of how tRNA works to bring amino acids to the ribosomes.
1) From seeing these videos, how would you define translation? Where is translation taking place—in the nucleus or cytoplasm? How are ribosomes involved in the process? How are tRNAs involved in the process?
Translation is when the mRNA strand is coded into a protein (my words). In translation, messenger RNA (mRNA) produced in transcription is decoded to produce a specific amino acid chain, or polypeptide, that will later fold into an active protein. Wikipedia. I suppose this is why I failed the BMB exam. This process takes place in the cytoplasm of the cell. Ribosomes decode the genetic information carried in the mRNA by coupling with the strand of mRNA by way of complementary base pairs. The tRNA carries specific amino acids which would then be coupled together in an elongated polypeptide strand.
2) The first segment also talks about protein processing. What can happen to a protein as it leaves the ribosome? How can it enter the rough ER? From the rough ER, where next can it go for processing? If a protein is packaged for secretion, what happens to it—how does it get to the cell membrane where it will be released?
The protein that leaves the ribosome through a vesicle will travel to the Golgi Apparatus and then be processed (except for insulin, the example in the clip, which doesn't get processed until it leaves the Golgi). It enters the Rough ER by way of the ribosome. The ribosome "docks" onto the rough ER and allows passage of the protein molecule. From the ER, it travels to the Golgi, where it will be processed (as I said already). The protein will travel to the cell membrane through vesicles and a predetermined pathway (if the video clip is to be believed).
3) The second segment reviews how tRNA works. What is tRNA? Which end of the tRNA molecule gets attached to an amino acid? What is an anticodon? Where is the anticodon on the tRNA? How is an anticodon used? Why is the tRNA for methionine so important?
tRNA is Transfer RNA. Transfer RNA (abbreviated tRNA) is a small RNA molecule (usually about 74-95 nucleotides) that transfers a specific active amino acid to a growing polypeptide chain at the ribosomal site of protein synthesis during translation. tRNA-Wikipedia. The 3' end. Anticodons carry the three complementary base pairs that will pair with the tRNA strand. The anticodon appears on the "bottom" of the tRNA molecule. Methionine is extremely important because it is the initiator codon: it jump starts the process of translation (I believe the base pair is AUG).
Lecture 26 (From Protein to Gene: Translation) Lecture Movie
Task 2: Lecture Movie on “From Gene to Protein: Translation” and Campbell Chapter 17 (pages 337-348)
Concept 1 – Review: Genes from one organism can be inserted into completely different organisms and be expressed, because the genetic code is universal!
1) How do we know that the genetic code is universal, i.e., that every organism can read the same genetic code?
2) How does the process of transcription and translation differ in a bacterial cell vs. a eukaryotic cell?
Concept 2 – Translation is the process whereby proteins are synthesized using the code that is on the
messenger RNA.
1) To translate a mRNA into a polypeptide, what specific components do you need?
Concept 3 – The work of Marshall Nirenberg cracked the genetic code. From his results, Nirenberg was able to figured out what nucleotides coded for what amino acids. He realized that 3 RNA nucleotides coded for a single amino acid. A group of 3 nucleotides, therefore, make up a codon.
1) What was Nirenberg’s experiment? Did he do this in living organisms or in a test tube? What components did he combine in his experiment? How did he figure out that there were three nucleotides in each codon?
2) How many possible codons are there? How many amino acids are there? Do all codons code for an amino acid? What codons function as stop codons? Do the stop codons also code for an amino acid? What codon functions as a start codon? Does the start codon also code for an amino acid? If so, which one?
3) Why do we say that the code is redundant? What does that mean? Why do we say that the code is not ambiguous? What does that mean?
4) What is a reading frame? Why is it important to be in the correct reading frame?
Concept 4 – To go from mRNA to protein, you need all the amino acids, tRNAs, lots of ribosomes, and of course mRNA.
1) Of the components listed above, which are made out of RNA?
2) How is tRNA used in the process of translation? How many amino acids is each tRNA specific for?
3) How are ribosomes used in the process of translation? Are ribosomes specific for specific mRNAs? Or can a ribosome read any mRNA that comes along?
Concept 5 – tRNAs bring the amino acids to the ribosomes. They have specific properties that make them able to do their job.
1) When you look at a tRNA, what shape is it? Where is the 3’ end of the molecule? The 5’ end of the molecule?
2) What is an anticodon? What is the function of the anticodon? Where on the tRNA is the anticodon?
3) Where does the amino acid attach to the tRNA? How many different kinds of amino acids can a single tRNA attach to? Is a tRNA specific for only a single amino acid? Or can it attach to several different types of amino acids?
4) What is a “charged” tRNA? How does the amino acid get loaded onto the tRNA? How is aminoacyl-tRNA synthetase involved in “charging” tRNA molecules? Is this synthetase specific for a single type of tRNA, or can each aminoacyltRNA synthetase charge several different kinds of tRNAs?
Concept 6 – Ribosomes are enzymes, made primarily out of RNA, that position themselves on the mRNA in order to translate the mRNA into a polypeptide.
1) Ribosomes are made up of two subunits. What is the function of the smaller subunit? What is the function of the larger subunit?
2) There are three different sites on the larger ribosomal subunit: E, P, and A. What happens at each of these sites?
Concept 7– There are three stages to translation: initiation when the ribosome finds where to start reading on the mRNA, elongation when the ribosome builds the polypeptide one amino acid at a time, and termination, when the stop codon signals the stop of translation and the ribosomal complex falls apart.
1) At initiation, which ribosomal subunit first attaches to the mRNA? How does it know where the start site is on the mRNA, i.e., what is the codon for “start”? Does this codon also code for an amino acid? If so, which one?
2) When in this process does the first tRNA dock onto the mRNA? Where does it dock? When does the large ribosomal subunit attach to the mRNA? How does it position itself in relation to the mRNA and in relation to the first tRNA?
3) How does elongation proceed? What is happening at the A site of the ribosome? At the P site? At the E site?
4) When the ribosome reaches a stop codon, what happens? How is the release factor involved? Where does the release factor sit?
5) How does the completed polypeptide chain get released from the ribosomal complex? Does every polypeptide, when it is first released from a ribosome, contain a methionine at one end? How do you know?
Concept 7– As a polypeptide chain is being made, it immediately starts folding into its secondary structure as soon as it is long enough to do so. The polypeptide can also start entering the rough ER before the polypeptide chain is finished being made.
1) What type of folding is involved in creating the secondary structure of a protein? What is an α-helix? What is a β-pleated sheet? What do we mean when we refer to the “tertiary structure” of a protein? To the “quaternary structure” of a protein?
2) How does a polypeptide get from the ribosome into the rough ER? What happens to the polypeptide in the rough ER?
Lecture 26 (From Protein to Gene: Translation) Post-Lecture
Task 3: Post-lecture Assignment – Two short articles, “Biotechnology: Bacteria Make Insulin” & “Resistance to Bt Crops Emerges”
Biotechnology is now a huge field that has grown up primarily because, as you learned in the Lecture Movie, the genetic code is universal, and we now know how to isolate genes from one organism and insert them into other organisms to create transgenic organisms. This use of biotechnology is also bringing up many ethical, legal, and safety issues. We will only probe into a small sample of these.
1) The first article explains three different uses of biotechnology. It also explains how we can take a human gene for insulin, insert it into bacteria, and get the bacteria to make human insulin. That insulin can then be harvested and used for diabetic patients. How is the insulin gene inserted into the bacterium (you only have to explain this in the same detail that the article does)? What do you think are some of the advantages to this technology? Can you see any disadvantages to the technology? Do you think this technology could increase antibiotic resistance in the common E. coli bacterium? Why or why not?
The article states how the most common way is to splice the plasmid of the bacterium so that it can be passed a-sexually from one bacteria to another. The advantages of this technology is that it could make life better. I mean, look at the example the article used of pesticides in plants. There is a certain pesticide (Roundup) that kills everything; plants included. But if plants (in this example, tomatoes) could be implanted with the genetic "booster" to make it immune to this pesticide, the pesticide would be effective and the plant will thrive. There are certain issues with biological research, though. It is possible to mutate the plants, animals and bacteria by "playing too much" with the DNA structure. But that could be focused more in the realm of science fiction. The realistic point I wanted to make here was under the same example of pesticides and tomato plants. Yes, it is true that you can genetically boost the immunity of the plant so that it is immune from being K.O.'d by Roundup..but such a thing might also have an effect on the pests themselves. If there are "pests" out there that the pesticide is fighting to control, it is possible for those pests to mutate and evolve to also be immune to the pesticide; so then there would have to be something more…and who's to say, also, that the evolved pest won't be more dangerous and toxic than the original?
I don't know if this type of technology could boost the resistance in the common E. coli bacteria. I suppose it could be possible. And I don't know why it's possible or not. I'm guessing, based on the way the question is worded and I could research it, sure…but since the final is tomorrow, I highly think that's……really pertinent. Do you?
2) The second article talks about genetically modified (GM) crops. The number of acres of GM crops planted worldwide is huge. There is a great deal of controversy over the use of GM crops. This article talks about corn and cotton crops that have been genetically modified to contain a bacterial gene that produces a toxin that kills insects. These crops are called Bt crops. What is the problem discussed in the article that has emerged with these crops? How have farmers tried to keep this problem in check? Do you see any advantages to using Bt crops? Do you see any disadvantages to using Bt crops?
The problem is that the pests the crops are supposed to act against are evolving to resist the toxicity of the plant. Farmers plant "normal" crops along with the Bt crops in hopes that the non-resistant individuals will mate with the resistant one and, hence, the resistance in the population can be controlled. Using Bt crops can help the Ozone layer. From what I remember hearing here and there, pesticides are a definite component in the whole global warming debate-thingy. So making GM crops that can kill pests without the need for air-born pesticides could help the environment.
(and global warming or not, it is possible for pesticides to spread and unfortunately harm things that weren't meant to be harmed).
And there are disadvantages; one being that the pesticides could potentially be harmful to humans and animals that might consume the plants.
Lecture 27 (From Protein to Gene: Transcription and Mutations) Pre-Lecture
Task 1: Pre-lecture Introduction –Two Videos: “Gene Mutations” & “A Review of Translation”
The first video has two segments on point mutations in DNA. The first segment gives you an overview of the process. The second segment is more detailed in explaining two types of point mutations: base-substitutions and frameshift mutations.
1) From seeing the first segment of the first video, how would you define mutation? What kinds of environmental substances can cause mutations?
Mutation is a change in the "normal" DNA sequence. Mutations can be caused by a number of things: chemicals (such as asbestos), cigarette smoke, radiation (from the sun or X-rays),…etc.
2) The second segment of the first video reviews specific types of point mutations. What is a base-substitution mutation? What can be the result of a base-substitution mutation? What is a frameshift mutation? What can be the result of a frameshift mutation?
It's pretty self explanatory. A base-substitution is when one base is SUBSTITUTED with another (hah. Imagine that.). The result could be 1) the coding for the wrong amino acid, or 2) it could produce a stop codon prematurely.
A frame-shift mutation is when a nucleotide sequence is added to the DNA strand. The result is that the whole amino acid coding is thrown off and can result in coding for the wrong amino acid because of the change in nucleotide reading.
3) The second video is a good review of translation. It shows the three stages of translation. What are these three stages, and, briefly, what happens in each?
Initiation: the mRNA moves to the ribosome where the smaller portion of the ribosome attaches itself to the mRNA strand and binds to the start codon (AUG). A tRNA molecule will then move in, binding to the mRNA strand with the complementary base pairs and is then "sealed" with the upper portion of the ribosome.
Elongation: The amino acids that are attached to the tRNA molecules form together through a covalent bond to create a polypeptide chain. This polypeptide chain elongates imagine that as each new tRNA molecule is added to the sequence. One tRNA molecule is added, the polypeptide chain is transferred to the newest tRNA molecule and then the first one ejects the ribosome…and this process is continued until a stop codon is reached.
Termination: A release factor binds to the stop codon on the mRNA strand and initiates the termination portion of this process. The polypeptide chain is released from the ribosome and the entire structure starts to break apart.
4) The second video also shows the different regions of an mRNA molecule in a eukaryotic cell, how a ribosome works, the different sites on a ribosome, and how transfer RNAs (tRNAs) work. The video does not name the E site on the ribosome, but implies its presence. What does it tell you about the P site on the ribosome? About the A site? What does the video tell you about tRNA molecules? What does the video tell you about mRNA?
Lecture 27 (From Protein to Gene: Transcription and Mutations) Lecture Movie
Task 2: Lecture Movie on “From Gene to Protein: Translation & Mutations” and Campbell Chapter 17 (pages 337-348)
Concept 1 – Cells tightly regulate where and when a gene gets expressed. There are many mechanisms that determine which genes will be turned on in which cells and at what times.
1) Why is it important that gene expression is regulated in cells? When we say a gene is expressed, what do we mean?
Concept 2 – Review: The genetic code can be summarized in a table of 64 codons, 61 of which code for amino acids, and 3 of which are stop codons.
1) How many nucleotides are in a codon? What is the function of a stop codon?
2) What does it mean to say the genetic code is redundant?
Concept 3 – Review: Aminoacyl-tRNA synthetase is an enzyme that attaches an amino acid to the end of a tRNA molecule. This is called charging the tRNA.
1) How many different kinds of aminoacyl-tRNA synthetase molecules are there? Why is it important to have this many?
2) Is energy involved in charging a tRNA molecule?
Concept 4 – Review: DNA, RNA, and polypeptides all have a directionality to their molecules that is very important to how they are put together and how they function.
1) What do we call the two different ends of a DNA molecule? Of an RNA molecule? In what direction is a DNA molecule synthesized? In what direction is an RNA molecule synthesized?
2) How do we refer to the two ends of a polypeptide molecule? When a polypeptide chain is forming, at which end of the molecule is the first amino acid? To which end of the molecule will the next amino acid be attached?
Concept 5 – Review: Termination stops the process of translation.
1) How does a ribosome “know” where it should stop translation when it’s moving down an mRNA molecule?
2) What is a stop codon? Are there tRNA molecules that correspond to the stop codons?
3) What is a release factor and how does it function? If a cell developed a mutation that prevented release factors from working, what do you think the result would be—would the cell survive such a mutation? What is your reasoning?
Concept 6 – Review: As the polypeptide is being threaded out of the ribosome, it starts folding up into its
secondary structure.
1) What do we mean by the primary structure of a protein? By the secondary structure? If the protein starts folding immediately into its secondary structure, what does that tell you—is this a process that requires energy or additional enzymes?
2) What is the tertiary structure of a protein? The quaternary structure?
Concept 7– Polypeptides are made in such a way that the cell can target them to go to specific places. For example, if the polypeptide is going to be processed for secretion, it enters the rough endoplasmic reticulum (rER).
1) How does a cell know that a polypeptide is to end up secreted from the cell? Where is the information that indicates this?
2) What is a signal-recognition particle, and how is it involved in getting a polypeptide to enter the rER?
3) What must a ribosome do in order to make sure the polypeptide it is making enters the rER?
Concept 8– Transcription and translation can occur simultaneously in a bacterial cell. You can get hundreds of ribosomes attached to a single mRNA molecule even before it has finished being transcribed.
1) Why can transcription and translation occur simultaneously within a bacterial cell?
2) Why doesn’t this happen in a eukaryotic cell?
3) In a eukaryotic cell, how are pre-messenger RNA molecules processed prior to leaving the nucleus?
Concept 9– A mutation is a change in the genetic information of a cell. So, it is any change in the nucleotide sequence in DNA.
1) How can a mutation lead to an altered protein?
2) What are some examples of things that can cause mutations, i.e., list some of the things we know are mutagens?
3) Sickle-cell anemia is a debilitating disease caused by an altered form of hemoglobin. What is the mutation that results in sickle-cell hemoglobin?
Concept 10– There are a number of types of mutations. In the Lecture Movie, we only cover types of mutations called point mutations. These can come about during DNA replication when one nucleotide gets replaced by a different kind, or an extra nucleotide is added, or a nucleotide gets deleted.
1) From the types of mutations listed above, which is a base-pair substitution? Which is a base-pair insertion? Which is a base-pair deletion?
2) Does a base-pair substitution change the reading frame? Does a base-pair insertion? Does a base-pair deletion?
Concept 11– A silent mutation is a change in the nucleotide sequence in the DNA that does not end up altering the sequence of amino acids in the protein.
1) How can a silent mutation come about—what is it about the genetic code that makes it possible for a mutation not to affect the sequence of amino acids?
2) Can you see any adaptive benefits to the redundancy in the genetic code?
Concept 12– A missense mutation is a change in the nucleotide sequence in the DNA that ends up putting in the wrong amino acid in a protein.
1) How can a missense mutation come about—what type of change in the nucleotide sequence will cause a missense mutation?
2) Can missense mutations be seriously detrimental? Could they sometimes have little effect on the protein? Explain.
3) What is a frameshift mutation? Can a frameshift mutation be a missense mutation? Explain.
Concept 13– A nonsense mutation is a change in the nucleotide sequence in the DNA that changes a codon into stop codon.
1) How can a nonsense mutation come about—what type of change in the nucleotide sequence will cause a nonsense mutation?
2) What can be the result of a nonsense mutation? Explain.
Lecture 27 (From Protein to Gene: Transcription and Mutations) Post-Lecture
Task 3: Post-lecture Assignment – Three short articles: “Sun Struck,” “Indoor Tanning Ups Skin Cancer” & “Sunny Solutions”
1) We all know, I’m sure, that UV light can cause skin cancer. The first article tells us that UV light primarily causes two types of skin cancer: basal cell and squamous cell carcinomas. (Please realize that skin cancer is very easily detected and effectively treated when caught early!) From this first article, what group of people is showing the greatest increase in incidences of these two skin cancers? Why do the researchers conclude that this increase is due in large part to full-body tanning?
The people who use tanning booths seem to have a higher risk of contracting skin cancer than those who have never used one (or use them infrequently. The article wasn't clear). Those who did tan in full-body tanning booths seemed to have a higher risk for skin cancer. That is all.
2) The second article tells us that indoor tanning increases our risk of skin cancer. What were the researchers estimates of this increased risk of skin cancer if we use indoor tanning?
Women: 30 in 100,000.
Men: 27 in 100,000.
3) The third article tells us about a study that added “snippets” of DNA to sunscreen. This new sunscreen seems to considerably reduce the damage from UV light. What “snippets” of DNA did the researchers add to the sunscreen? Why do you think this worked? How does UV light damage DNA? Do you think this is related to the choice of DNA snippets used by the researchers?
Thymidine dinucleotide (pTT). It works because pTT is a substrate for thymine dimers which…do something….with skin…..I dunno. There was a table and a picture-like thing. UV light damages DNA because it…just fucking does, you mother fucker.
Lecture 30 (Evolution & Genomics) a Pre-Lecture
Task 1: Pre-lecture Introduction – Video: “The Human Genome Project: Cracking the Code”
The Human Genome Project was a huge international effort to sequence the entire human genome. The story of this project includes competition and controversy, and the ramifications of its outcome are only beginning to be felt.
1) When did the project begin? When did it finish? Why did it finish ahead of schedule? How much money was budgeted by the United States government for the project?
The project began in the '90s? It finished in about 3-4 years; over a decade before they had planned on finishing. It finished ahead of schedule because severe competition arose; the Great Gene Race. 3 billion dollars was budgeted over 15 years for the project's completion (roughly one dollar/bp).
2) Francis Collins and Craig Venter were two key figures in the project. What were their roles?
Francis Collins was on the side of the public science domain; the one who was pushing for open source of genetic information. Craig Venter ("Darth Venter") was on the side of a private company called Celera, which was pushing the public domain to sequence the DNA.
3) What ethical, legal, or social issues can you think of that might have arisen in the aftermath of the Human Genome Project because of all these new data we now have about the human genome?
Well it was obvious in watching the video that the people who presented the information were very much against the Celera company. Either way, some of the things that Celera was doing could be considered unethical. For example, they agreed to open source their genetic findings, but not before they held onto their discoveries for a while and even patented some of the genome. They also wanted scientists and even the government to pay them to use their services in sequencing DNA. Personally, I think that's wrong because science should not ever be about money. Science should help people understand their word and, in the genetic sense, help locate genes that might cause diseases. But putting a price tag on such information inhibits the spread of knowledge. That, and it's mother fuckin' greedy.
I think it's also kinda immoral to try and patent DNA sequences. You didn't freakin' come up with it. >< Billions of years of EVOLUTION came up with it, you sonuvabitch.
On the other hand, the open-source scientists were not wholly in the light, either. It was through the competition with Celera that the HGP was accomplished as quickly as it was, but that meant that it could have been accomplished well under the 15 year mark, regardless of competition. And Venter was quoted in saying that a lot of the OP scientists were planning on retiring after their research in this project. So they were planning on living off our tax dollars for much longer than they could have been?
Lecture 30 (Evolution & Genomics) Lecture Movie
Task 2: Lecture Movie on “Genomes and Their Evolution” and Campbell Chapter 21
Concept 1 – Analysis of genomes provides data that can be used to figure out evolutionary relationships. New fields of study that analyze genomes have arisen as new technologies are developed for sequencing genomes. Two of these new fields are genomics and bioinformatics.
1) How would you define the field of genomics? How would you define the field of bioinformatics?
2) When did these two fields get started? What happened in the 1990s that really accelerated progress in these fields?
Concept 2 – The Human Genome Project was a huge, collaborative, multinational effort to sequence the entire human genome. It started in 1990 and was projected to take 15 years, but it actually was completed ahead of schedule in 2003.
1) Why was it possible for the Human Genome Project to finish ahead of schedule?
2) What is the shotgun method for genome sequencing? Who invented it, and what company did he start (hint: see your textbook, page 428)? When did he start this company? Why did this method propel the Human Genome Project forward so fast?
Concept 3 – The new efficient methods for genome sequencing have led to many genome projects: e.g., the Mouse Genome Project, the Canine Genome Project, the Feline Genome Project, the Bovine Genome Project.
1) The genomes of many organisms have how been sequenced. What are five of these organisms? Have the genomes of any invertebrate species been sequenced, and if so, what is at least one of these? Have the genomes of any plant species been sequenced, and if so, what is at least one of these?
2) Can you get access to any of these sequence data? Where are the databanks containing all these data?
3) If you were studying an organism and isolated a protein from this organism, and figured out what the amino acid sequence was of this protein, how could you use these databases to figure out what protein you had isolated. What types of information could you get from a Web search?
4) Poke around on the Web. You can go to the National Center for Biotechnology Information (http://www.ncbi.nlm.nih.gov/). Choose a BLAST search from the right-hand menu. Go ahead and do a search. Create your own query sequence. You can make up a nucleotide sequence or an amino acid sequence, or use one from your textbook, and just see what you get. Here’s the amino acid query sequence that the book used as an example—you can use this if you’d like, just copy it and paste it into the query line —
~~~ktGGIRL~RHfksVSAVEWHRk~~gDYLSTlvLreSRAVLIHQlsk If you entered this sequence and did a protein blast, what did you find out about the protein? Did you figure out what kind of protein you’re probably dealing with?
Concept 4 – Proteomics is a new field that compares full sets of proteins from different organisms. It looks at when and where proteins are produced and how they interact.
1) How is proteomics being applied to fields such as medicine?
Concept 5 – When comparing the genomes of different organisms across the 3 domains of life (bacteria, archaea, and eukaryotes) there are some broad conclusions you can draw: bacteria have the smallest genomes and the smallest number of genes; the genomes of eukaryotes are much larger; the genomes within the eukaryotes vary considerably in size, and yet the number of genes in these different eukaryotes hovers around 20,000 genes.
1) What conclusions can you draw from the very small genome size of the bacteria?
2) What conclusions can you draw from realizing that a nematode worm has about the same number of genes in its genome as humans do in their genome?
3) What conclusions can you draw from realizing that a plant such as the lily Fritillaria assyriaca has a genome size that is over 37 times larger than that of humans?
Concept 6 – In looking at the human genome, we see that most of the genome is taken up by repetitive DNA that is not part of the genes and does not code for proteins. In fact, only about a quarter of our genome is tied up in genes, and most of this is taken up by introns—only about 1% of the human genome is represented by exons coding for proteins!
1) What do you think all this “extra” DNA is doing?
2) What are transposable elements? Who discovered transposable elements (“jumping genes”)?
Concept 7– Many genes code for similar proteins, and we have now realized that these represent multigene families—i.e. genes that in the evolutionary past started out as a single gene, but through duplications and mistakes in DNA replication, eventually evolved into separate genes making slightly different proteins with different functions.
1) What are some examples of multigene families?
2) How would a multigene family crop up? Look at Figure 21.13. What were the probable steps in the evolution of the human α-globin and β-globin gene families?
Concept 8– We can use comparisons between genome sequences to determine evolutionary relationships and figure out when various species diverged.
1) Why can we use sequence differences to estimate how far back in evolutionary history two species shared a common ancestor?
2) Look at Figure 21.15. How many billion years ago is it estimated that eukaryotes and archaea diverged from a common ancestor? How many years ago did humans and chimpanzees diverge from a common ancestor?
3) What is the percent difference between the human and chimpanzee genomes? What does this tell us about the importance of controls of gene expression for determining phenotype?
Concept 9– The field of evo-devo (evolution and development) studies the evolution of embryonic development and patterns of gene expression within developing organisms (i.e., when and where genes get turned on and off).
1) What are homeobox genes (also called homeotic genes)?
2) Why can a mutation that affects a homeobox (homeotic) gene have a major effect on the morphology of an organism?
Lecture 30 (Evolution & Genomics) Post-Lecture
Task 3: Post-lecture Assignment – A Video: “Patenting Genes: A Gene Controversy” & an Article “The Lawsuit Against Myriad”
1) The Human Genome Project followed by the rise in genomic sequencing technologies have caused a rush to the patent office by research labs and companies to patent any genes they isolate. Now, 20% of all human genes have been patented! This has gone unchallenged in the courts until just recently, when a lawsuit was brought against the company Myriad, which holds the patent for two breast cancer genes, BRCA1 and BRCA2. The mutated forms of these genes greatly increase a woman’s risk of developing breast cancer and ovarian cancer. Anyone who needs to be screened for the mutated forms of these genes must use the testing facilities at Myriad.
1) What are the arguments being used against Myriad? What are the arguments Myriad is using in its defense? What is your own opinion in the case?
The arguments against Myriad are that genes should not be patented because it is unconstitutional. Myriad says that, if it wasn't for patents, there would be no way of pushing forward cures for genetic diseases, including cancers. I don't think genes should be patented because it is something that occurs naturally, they did nothing but find it (and that makes no sense. There's no "finders fee" in science. ><) and it makes the flow of information more choppy and disambiguous. Science should be openly available and accessible, not for used solely for monetary gain.
2) If Myriad loses this case, what do you think the ramifications will be for researchers? For biotechnology companies? For the health system?
I don't know if there would be any ramifications for the researchers. Do you mean the researchers who performed the tests and found the gene, or the researchers in the public sector? Because as for the latter, one, I see no harm that could befall them (in the very least, not in comparison to the ramifications already in place). The biotech companies will have a serious hit because they are already trying to patent genes and DNA sequences…so if Myriad falls, a lot of other biotech companies would be looked into. It could very well be a domino effect. The health system would get a boost because then the sharing of information could become available, more efficient and better tests could be made, the gene could have a cure….and people would be able to pay for the testing for such a gene if necessary. Monopolies are illegal, so why is it legal or even moral for these companies to literally monopolize a certain gene?
Lecture 31 (Evolutionary Arms Race) Pre-Lecture
Task 1: Pre-lecture Introduction – Video: “Extremely Drug Resistant Tuberculosis”
Tuberculosis (TB) is a devastating disease—and drug resistant forms of it are on the rise. The World Health Organization (WHO) calculates that 9 million people have TB today, and it kills 1.6 million every year. The rapid evolution of drug-resistant forms is of particular concern. TB is caused by a bacterium, and for most forms of TB, a 6- month course of antibiotics eradicates the disease
1) Why are antibiotic-resistant strains of TB evolving?
They are evolving because the disease is continuing to spread. It also has to deal with the regiment of medication. The video mentioned that a lot of the patients who have contracted TB take their medication…but don't stay on it. This kind of behavior allows for the surviving strands of TB to evolve and build up a resistance to the once-effective drug and continue to spread.
2) How is the increase in numbers of AIDS cases affecting the number of TB cases?
She didn't say why; she states that the increase in HIV (which is different than AIDS, btw) correlates with the increase in TB cases.
3) How much would it cost to control TB, worldwide? (Hint: about the same amount as it costs the United States to support the wars in Iraq and Afghanistan for 2 days, or the amount that is spent on pharmaceuticals in one day in the United States, or the amount that the movie “Avatar” has made in domestic sales since it’s been out.)
The movie said an additive 250 million dollars (give/take); added to the already growing global budget for this program.
Lecture 31 (Evolutionary Arms Race) Lecture Movie
Task 2: Lecture Movie: A PBS Production—“The Evolutionary Arms Race” & pp. 460-461 in Chapter 22
Concept 1 – The bacterium that causes tuberculosis has been evolving into multidrug resistant forms. There is a sharp rise in multidrug resistant forms of TB in Russian prisons, and these are now showing up in the general population.
1) What has been causing the selection of these drug-resistant forms of TB?
2) How is TB spread from person to person? What conditions promote the spread of TB? What are the conditions in Russian prisons that favor the spread of TB?
3) Have drug resistant forms of TB spread to the United States from Russia? How do we know?
Concept 2 – E. O Wilson tells us, “Evolution is driven not just by physical forces, such as storms and fire and climatic change, but much more by biological forces, that is, particularly by the way species interact with one another—cooperating with one another, parasitizing one another, preying on one another.” As the movie summarizes it, “The deadly dance of predator and prey drives evolution.” A dramatic example of this involves a small salamander that secretes a toxin so potent a tiny drop on the tongue will kill a
person.
1) The rough-skinned newt (a small salamander found in western Oregon) produces a deadly toxin in its skin. How did people first figure out that this salamander was so toxic?
2) Why is this salamander so toxic? What is driving its evolution to ever more toxic forms? How is the garter snake involved in this evolution? How has the garter snake evolved in response to the ever more toxic forms of salamander?
Concept 3 – A new theory put forward by Paul Ewald at Amherst says that we can drive the evolution of pathogens to milder forms by knowing about their patterns of evolution. Ewald has noticed that pathogens spread by close contact between people tend to be mild, because they depend on people being relatively healthy to spread. But pathogens spread by feces in contaminated water or by insects tend to be severe. Ewald says we can domesticate these severe disease organisms just as we have domesticated other
organisms.
1) Cholera is typically a severe disease. How is cholera typically spread?
2) What has been done in certain areas to force cholera to evolve into milder forms? Did this take expensive medical procedures? Do you think it was an expensive method of disease control?
3) What evidence from cats indicates that we might also be able to push the evolution of HIV to milder forms.
Concept 4 – Symbiosis affects the evolution of species. Species that are dependent upon each other for survival are driving forces for each other’s evolution—they coevolve. Examples include flowers and the bees that visit them, plants and the fungi that extract nutrients from the soil for them, humans and the bacteria on our skin and in our gut that protect us from pathogenic bacteria and aid in our digestion. These relationships seldom involve only two species, however. The long-term study of leaf cutter ants gives us an excellent example of this; it also shows us how we as scientists are often blind to the complexity of interspecies interactions.
1) Leaf cutter ants cut leaves and bring the pieces of leaves back to the nest. What then happens to these leaves? Do the ants eat the leaves? Do the ants feed the leaves to another organism? If so, what organism, and what do the ants eat?
2) When studying this example of symbiosis, scientists first only saw two species involved in the relationship. What were
these two species? What were the scientists missing?
3) Why are there no “weeds” or contaminating molds found in the leaf cutter ants’ gardens? How are contaminating molds kept under control? Who discovered this? Was it a seasoned old scientist, or a young graduate student who refused to listen to his elders?
4) Why haven’t the molds in the ant gardens developed a resistance to the antibiotics used to kill them?
Concept 5 – Western cultures tend to think of all bacteria as enemies. But being “too clean” actually causes some health problems—allergies, for example, may be the result of not being exposed to enough microbes during early childhood.
1) What study is being done in Bavaria (a region of Germany) that indicates allergies may be a result of being too clean during early childhood?
2) What other evidence is there to show this is probably the case? Where are allergies on the rise, for example?
Concept 6 – E. O. Wilson states, “It is a big mistake for humanity to separate itself from the rest of the living world too much. The vast majority of species out there are our friends, they’re not our enemies. And we not only benefit from them, but as a whole they are essential to our existence. We’re the fortunate heirs of more than 3 billion years of evolution that created this stupendous diversity. We need to learn a lot more about the living world and the way that humanity itself is affecting evolution.”
1) What do you think Wilson means when he says that it is a big mistake for humans to separate themselves from the rest of the natural world?
2) What arguments can you make for studying evolution and the complex interactions among different species?
3) Wilson says that diversity is “essential to our existence.” What is an example of how humans are destroying diversity? What is an example of how humans are trying to preserve diversity?
Concept 7 – The movie states, “Like all living things humans are a product of evolution, but we’re the only species that knows it. We alone can see into the distant past and marvel at the history of life. We alone are beginning to understand that we can use evolution to shape the future for all of life.”
1) What is an example of how humans have shaped future evolution in a way that threatens our species?
2) What is an example of how humans have shaped future evolution in a way that will help our species?
3) What do you consider to be the most important thing we can do to “shape the future for all of life.”
Lecture 31 (Evolutionary Arms Race) Post-Lecture
_Task 3: Post-lecture Assignment – A Video: “How Do We See Biodiversity”
1) E. O. Wilson is a renowned biologist who has been a powerful voice for conservation and preserving biodiversity. This short video summarizes what he describes as the “human juggernaut” that is eroding our biosphere. He uses the acronym HIPPO to summarize the 5 major problems that humans have created.
2) What does “juggernaut” mean? (Use the Web or a dictionary to look it up if you don’t know.) What does Wilson mean by “the human juggernaut that is eroding our biosphere”?
3) What are the 5 major problems that Wilson is referring to with his acronym HIPPO?
4) An example of endangered species discussed in the video-clip are bats threatened by the disease white-nose syndrome? Where is this disease prevalent? Do we have it in Maine? Scientists don’t yet know the cause of this disease. What has been one suggestion for the cause? (Use the Web to find your answers.)
5) Use the Web to find out more about E. O. Wilson. Where has he been working for the past 50+ years? What
organism has he studied intensely? What is one of Wilson’s major pleas to the rest of us?
