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Lecture 22 (Chromosomal Inheritance) Pre-Lecture

Task 1: Pre-lecture Introduction –Video “Do Genetic Screenings Make Healthy Babies” & Article “The Universe of Genetic Testing”

1) We are entering an age of tremendous possibility when it comes to knowledge about our own genomes. How useful will all this information be? This video and article discuss some of the issues.
This information could become very useful — depending on how said information is utilized. It can be used to find genetic diseases or disorders that either you or your offspring will have in the future.

2) The short video talks about a couple who is choosing to get genetically tested prior to having a child to determine if they are carriers for any genetic diseases. What type of sample does the couple need to give for this test: blood, saliva, or urine? How much does the test cost? How many diseases does it test for, and how many mutations is it screening for? What is your own opinion of this sort of testing?
Saliva testing. Test costs ~$350/sample. It tests for 109 diseases (like Tay-Sachs and Sickle-Cell Anemia) as well as more than 400 genetic mutations. I think it's a good idea. I mean, people should be knowledgeable about it and even cautious about the testing, but it still seems justified to get screening done before having children.

3) The short article discusses the pros and cons of genetic testing. What are some of the pros and cons? Can the test tell you whether a person will definitely develop a disease, or the severity of the disease? Why or why not? Do you see any legal or privacy issues that can arise from genetic testing? For example, do you think an employer should be allowed to insist on genetic testing before hiring a person? Why or why not? What advantages could there be? What disadvantages?
PROS: Getting genetic testing done can tell you if you have a probability of getting a disease. It can also predict if such a disease might be passed onto your potential offspring.
CONS: Although the testing can look for certain genetic diseases, the testing only looks for certain abnormalities in the genes that cause the disease; not every gene that could cause it. Also, it only gives you a probability of getting a disease; so it's difficult to know if the symptoms would even present themselves, or even how severe said symptoms would be. There also could be some issues with patient privacy in these tests.
There could be definite advantages (like mentioned above) in knowing if there is a chance you or your offspring might be at risk for a certain genetic disease. But, as with everything, this type of testing should not be done lightly. There is a lot to consider before going in for this kind of test.
Also, the article in question made a mention that there could be a possibility of privacy breaching, but I am not really sure what the case would be where there would be such an issue (although the article did suggest a conflict with getting insurance to cover the testing). I can only assume that such a genetic testing could make it more difficult to receive/apply for insurance. Although such a thing shouldn't be all that difficult now, with national health care and all.

Lecture 22 (Chromosomal Inheritance) Lecture

Concept 1 – Thomas Hunt Morgan studied the inheritance of eye-color in fruit flies. He figured out that a mutation called white-eye is linked in some way to sex determination, since in most of his breeding experiments, only males ended up with white-eyes. Since it had already been established that sex determination involves chromosomes, Morgan’s work indicated for the first time that genes must be physically located ON chromosomes. It seems so obvious to us, now, but back then this was an incredible discovery—and it earned Morgan the Nobel Prize.

1) What experiment did Morgan set up using a true-breeding red-eyed female fruit fly and a white-eyed male fruit fly? What results did he get in the F1 generation? When he mated two individuals from the F1 generation, what were his results in the F2 generation?
Morgan set up an experiment trying to determine the heredity of the "mutant" white-eyed gene. In the F1 generation, Morgan found that all the offspring had red eyes — pointing to the probability that the red eyed gene was dominant. In the F2 generation, 75% of the offspring were red-eyed and only 25% were white-eyed; also interestingly enough, the white-eyed gene only seemed to show itself in the male.

2) The trait that Morgan was following is X-linked. What does that mean? In these studies, why did male flies exhibit white eyes, but female flies did not?
X-linked simply means that the allele for eye color was found on the X-chromosome of the flies. It was more probable that the males would exhibit the trait for white eyes because they only have one X-chromosome (whereas females have two). And since eye color is X-sex linked, it is more likely that males will express the eye color than females (being that the red eye color is dominant over white)

3) What does “hemizygous” mean, and how would you use the term in this set of experiments? Create a sentence that uses the term “hemizygous” to refer specifically to one of the animals in Morgan’s study.
"A diploid organism is hemizygous for a particular gene when only one allele for the gene is present" Hemizygous on Wikipedia
An example of this from the lecture was of grasshoppers who had an X-0 system in chromosomes.

4) Is it possible to obtain white-eyed female fruit flies? What genotypes would you cross in order to obtain white-eyed females? In your cross, how many of the female offspring in the F1 generation would be expected to have white eyes? How many of the male offspring in the F1 generation would be expected to have white eyes?
It is possible to have females with white eyes. You would have to select a male with the white eyed gene and a female who was heterozygous for the white-eyed gene. There would still only be a 25% chance that there would be a female offspring with white eyes, but it is entirely possible.
And in the F1 generation, 50% of the progeny will be white-eyed (while the other 50% will include a male homozygote for red eyes and a female heterozygote).

Concept 2 – In biology, certain organisms are chosen to be “model organisms” for scientific studies because they have attributes that make them easy to work with.

1) What are some of the attributes that make an organism a good candidate for being a “model organism”?

2) What specific model organisms does the Lecture Movie show you when it discusses what makes a good model organism?

Concept 3 – In the chromosomal systems of sex determination, we find that in mammals, the presence of a Y chromosome determines maleness: 2 X chromosomes result in females; 1 X and 1 Y chromosome result in males.

In this chromosomal system of sex determination, what would an individual be who is XX—male or female; who is X0 (has only one X chromosome); who is XXY (2 X chromosomes and 1 Y chromosome); who is XYY (1 X chromosome and 2 Y chromosomes)? (Note: these are all viable conditions that exist in human populations. They exist because errors in meiosis can lead to gametes that carry an extra sex chromosome or are missing a sex chromosome.)
XX: (normal) female.
X0: A female who is missing a second X chromosome. It's called Turner's Syndrome. Some of the symptoms include: webbed neck, short stature, low-set ears and may be at risks for such diseases like autoimmune diseases and diabetes, congenital heart disease, etc. They are also usually sterile, seem to have high infant mortality rates and most do not have a menstrual cycle. Occurs in roughly 1: 2500 girls. Turner's Syndrome
XXY: male who has 47 chromosomes and has an extra X chromosome. The symptoms are usually smaller testicles and decreased fertility and effect roughly 1:1,000 males. The symptoms range from each individual. Klinfelter's Syndrome
XYY: Occurs in males and is an aneuploidy. There doesn't seem to be many abnormalities in association with this karyotype, in that there are no phenotypical problems with having an extra Y chromosome. The only downside to having this specific karyotype might be that there is a chance of having a slightly lower IQ than your siblings if you have the extra Y chromosome, and you might have a learning disability (1:10) but nothing that completely keeps that individual from being "normal". The estimate of males affected with this extra chromosome are unknown because many men don't even know they are in possession of it. More information: XYY Syndrome

Concept 4 – There are many other chromosomal systems of sex determination: grasshoppers have a system called X-0; birds have a system called Z-W; ants and bees have a system called haplo-diploid.

1) In grasshoppers, what combination of chromosomes result in producing a female? In producing a male?
Female: XX; Male: X0

2) In birds, what combination of chromosomes result in producing a female? In producing a male?
Female: ZW; Male: ZZ

3) In ants and bees, how are females determined? How are males determined?
Female: Diploid (32 chromosomes); Male: Haploid (16 chromosomes)

Concept 5 – X-linked disorders in humans: certain diseases are due to mutations in genes on the X chromosome. These diseases are usually caused by recessive alleles and affect more males than females.

1) What specific diseases or conditions are listed in the Lecture Movie that are due to recessive alleles on the X chromosome?
Hemophilia and color blindness (especially the latter one) were two of the diseases mentioned in the lecture movie.

2) In your own words, why do these conditions primarily affect males?
Females have two X chromosomes whereas males only have one. Hence, if a female is heterozygous for an X-linked allele, the dominant one would show over the recessive trait. However, males don't have that ability to be heterozygous for a trait because they only have one X chromosome. So if they happen to receive the X chromosome with the recessive trait on it, they will show the trait.

3) If there is a couple in which the woman is homozygous for the dominant trait of normal vision, and the man is colorblind, what is the probability that a daughter of theirs will be color-blind? The probability that a son of theirs will be color-blind?
None of their children will be color-blind, although 50% of their progeny (both females) will be heterozygous.

4) If there is a couple in which the woman is heterozygous for the trait (i.e., has normal vision, but is a carrier for colorblindness), and the man has normal vision, what is the probability that a daughter of theirs will be color-blind? The probability that a son of theirs will be color-blind?
75% of their progeny will have normal vision when 25% of their offspring have the probability of being colorblind (male only). 50% of their progeny will be heterozygous.

5) If there is a couple in which the woman is heterozygous for the trait (i.e., has normal vision, but is a carrier for colorblindness), and the man is color-blind, what is the probability that a daughter of theirs will be color-blind? The probability that a son of theirs will be color-blind?
There is a 50/50 split with the offspring, two being color-blind (female and male) and 25% of a male having normal vision and 25% female offspring being heterozygous for the trait.

6) If there is a couple in which the woman is color-blind and the man has normal vision, what is the probability that a daughter of theirs will be color-blind? The probability that a son of theirs will be color-blind?
Like the last one, this one is also a 50/50 split. 50% chance the offspring will be male and be color-blind; and 50% chance that the offspring will be female and heterozygous.

7) If there is a couple in which the woman is color-blind and the man is also color-blind, what is the probability that a daughter of theirs will be color-blind? The probability that a son of theirs will be color-blind?
There is a 100% chance that the offspring of this couple will be color-blind.

Concept 6 – In female mammals, if both X chromosomes were active in each cell, there would be too much gene product being made. To control this dosage problem, one X chromosome in each cell is inactivated. This inactive X chromosome is called a Barr body.

1) In female mammals, the cells turn off (inactivate) one of the X chromosomes, by packaging it up tightly into a Barr body. At what stage in development does this occur? Does each cell turn off the same chromosome, or is it random?
I am pretty sure it occurs in Meiosis I, but I'm not positive

2) Explain how X-inactivation can result in the mottled coloring that we see in calico cats. Would it be rare to find a male calico cat? Explain. Can you think of a mechanism that could result in a male calico cat? (Hint: look again at your answers to the questions asked for Concept 3, above.)
X-inactivation works so that female mammals do not have more genetic material than the male counterparts (X chromosomes contain a lot of genetic material, while Y chromosomes carry very little information). This process occurs randomly in each cell of the body and, in the case of calico cats, presents the mosaic on the fur. It would be very rare to find a male calico but, as in the case of seeing a female who's color-blind, it's not impossible.

Concept 7 – Genes carried on the same chromosome are said to be linked, because they travel together when the chromosomes are moving around and are inherited together when passed on to the next generation.

Genetic recombination occurs during crossing over events in meiosis I; this genetic recombination can switch an allele from one chromosome to a homologous chromosome. How can you detect this crossing over in a breeding experiment? Study the example on the Lecture Movie and in your book that shows a cross between true-breeding fruit flies, one wild type and the other a double mutant with a black body and vestigial wings. Carry the cross through the F1 and F2 generations. How do the results of this experiment show that the b and vg genes are on the same chromosome? How do the results show that there can be recombination between these two genes during meiosis? How can you use these results to state how far apart the genes are from each other on the chromosome they’re on?

Lecture 22 (Chromosomal Inheritance) Post Lecture

Task 3: Post-lecture Assignment – One short article “Genetics of Muscular Dystrophy” & one short video
“Muscular Dystrophy: An Interview with Carl & Possible Cure through Gene Therapy”

1) Why is it mostly boys that are affected by this disease? Is it possible for a girl to be affected? What genotype for the
dystrophin gene would the biological parents need to be for a girl to inherit the disease?

Males are mostly affected because the allele for Muscular Dystrophy is on the X-chromosome. And being that males only have one X-chromosome, it is easier for recessive alleles to be expressed in males over females. It is possible for females to get the disease; but only if the father is a carrier and the mother is either a heterozygous carrier or homozygous carrier for the disease.

3) The short video shows a young man, Carl, with Duchenne muscular dystrophy, and then shows a new technique that is
in trials for curing the disease. Is Carl able to eat or walk? Why or why not? How long is a person expected to live
who has Duchenne muscular dystrophy? The type of cure discussed in the second part of this video is gene therapy.
How are the researchers delivering the “good copy” of the dystrophin gene to the cells of the patient?

Carl is unable to talk OR walk because the disease has deteriorated all his muscles. Carl states the average life expectancy is something like 19 years. They are injecting the "cure" into the muscle cells directly in an effort to enhance the productivity of the cell and perhaps even heal the cell.

Lecture 23 (Molecular Inheritance I) Pre-Lecture

Task 1: Pre-lecture Introduction –Video “TED Lecture: James Watson-The Double Helix”

This video shows James Watson as an elderly man talking about his work when he was a young man at Cambridge
University in England, where he worked with Francis Crick. Together they put forward the model of the structure of
DNA that still stands, today. The most important thing you can get from this video is the experience of hearing and
seeing this person who has made such a mark in modern biology.

1) At what age did Watson go to college as an undergraduate? When he decided to go to graduate school, what was his
first choice school, and did he get into his first choice school? Where did he end up attending college?

Watson was an undergrad at the age of 17 because Chicago allowed high school students to go to college after just two years in HS. His first choice in grad school was CalTech, but they turned him down. He ended up going to college in Indiana where, he said, they also had a wonderful genetics program as well as a good basketball team.

2) Key to the unraveling of the puzzle about the structure of DNA was having clear pictures of the molecule using x-ray
crystallography. Whose pictures of DNA did Watson and Crick use to decipher the structure of DNA?

If I remember correctly, the crystallography pictures were those of Rosalind Franklin.

3) Was the importance of Watson and Crick’s discovery immediately obvious to other scientists? What does Watson say
that indicates their work was largely ignored for the first five years after it was published? What were the reasons that
Watson gives for it being ignored?

The importance, I don't think, was completely obvious to the whole scientific community. I mean, it was obvious because Watson and Crick weren't THE ONLY ones working on the structure and make-up of DNA. There were several other scientists (even a couple that Watson mentioned by name) that were "racing" to discover the structure. But, as I recall, there were also a number of scientists who believed that the genetic code was contained in proteins (which is a little funny because DNA codes for proteins…). But I think there was a little resistance in the scientific community as a whole because they (as Watson put it) tended not to believe things unless they were definitely true. Watson made the point in saying their findings on the structure were 95-99% true, so he didn't understand the struggle with getting their work openly accepted by the community.
He also made mention that, in five years, there were very little references to his and Crick's work on DNA.

4) From watching the video, what are your impressions of Watson?
He is a very quirky old man with a good sense of humor. He is also really intelligent (although I don't know if some of that feeling of "being in awe of his intelligence" has more to do with himself or what he did to discover the structure of DNA with Francis Crick) and highly skilled.

Lecture 23 (Molecular Inheritance I) Lecture

Task 2: Lecture Movie on “Molecule Basis of Inheritance - I” and Campbell Chapter 16

Concept 1 – We already know in this class more about DNA than any of the scientists who were studying it, when they were trying to work out the structure of DNA.

1) In the Lecture Movie, the pictures of several scientists are shown who worked on the structure of DNA? What are the names of these scientists?
Worked on the actual structure or helped collectively discover what DNA is?
1) T.H. Morgan
2) Watson & Crick
3) Frederick Griffith
4) Avery, McCarty, MacLeod
5) Hershey and Chase
6) Erwin Chargaff
7) Rosalind Franklin
8) Maurice Wilkins

2) What 5 things are listed in the Lecture Movie as things that you already know about DNA?

  • DNA is made up of proteins and nucleic acids
  • DNA has 4 base pairs
  • DNA strands run anti-parallel
  • DNA has phosphate groups and sugars on the outside of the helical strands
  • DNA carries the genetic code for all organisms

Concept 2 – Watson and Crick published their model for the structure of DNA in 1953, in a one-page paper in the journal, Nature.

1) What did Watson and Crick build their large model of DNA out of?

2) Where can you go to see the actual model that they built?
Museum of Science in London, England.

Concept 3 – Searching for the genetic material: a) there was a great deal that Watson and Crick needed to know before Watson and Crick could create their model of the genetic material. The first thing scientists needed to do was to determine what exactly the genetic material is. Many key experiments contributed to the discovery that the genetic material is actually DNA.

1) What contributions did the work of T. H. Morgan make to unraveling the puzzle of what constitutes the genetic material?
He showed that a gene was on a chromosome.

2) What did people know about chromosomes at the time, i.e., what did they know about what chromosomes were made up of?
Chromosomes are made up of nucleic acids and proteins

3) What two substances were being tested for possibly being the genetic material?
Proteins and nucleic acids

Concept 4 – Searching for the genetic material: b) Frederick Griffith, in trying to create a vaccine against a bacterium that causes pneumonia, stumbled on a great model system that could be used to test whether the genetic is DNA or protein. He did not go on to do these experiments, however, but another group of scientists did, Avery, McCarty, and MacLeod.

1) What experiment did Griffith do? When he injected mice with the S strain of bacteria (the pathogenic strain), what happened to the mice? When he injected mice with the R strain of bacteria (the non-pathogenic strain), what happened to the mice?
Griffith did an experiment on a bacterial strand of Pneumonia. When mice were injected with the S strand, they died. When they were injected with the R strand, they lived.

2) When Griffith first heat-killed the S strain of bacteria and injected mice with these, what happened to the mice? When he injected mice with heat-killed S bacteria along with living R bacteria, what happened to the mice? How do you interpret the results of this experiment? The results were an illustration of transformation. Why is this called transformation?
When Griffith injected the heat-killed S strain into the mice, the mice lived. When he injected heat-killed S strain and R strand into the mice, the mice died. The DNA from the S strand "moved" into the R strand and caused them to transform into the killer S strand.

3) Scientists now simply needed to figure out what had passed from the dead S bacteria to the living R bacteria that changed the R bacteria into the pathogenic form—whatever that substance was, that would have to be the genetic material. What were the three possible candidates for this material, based on the results of the experiment?

  • Proteins
  • DNA
  • …dunno the third one.

Concept 5 – Searching for the genetic material: c) Avery, McCarty and MacLeod built on the work of Griffith, and their results clearly showed that the genetic material is DNA. But other scientists did not believe their results.

1) What did Avery, McCarty and MacLeod do in their experiments using S and R strains of bacteria?

2) What were the results of their experiments? How did these results indicate that the genetic material was indeed DNA?
They found that it was DNA that changed the non-lethal R strands from S strands.

3) Why didn’t other scientists believe the results of these experiments?
Because scientists are skeptical. They also didn't believe it because DNA only contains 4 nucleic bases, whereas proteins have 20 amino acids. They believed DNA was too simple to contain all the genetic material needed for all organisms.

Concept 6 – Searching for the genetic material: d) Experiments by Hershey and Chase nailed it—their results clearly showed that DNA is the genetic material, and this time other scientists believed the results.

1) What system did Hershey and Chase work with? What is a phage virus? Why is it a perfect system to work with to figure out whether the genetic material were protein or DNA?
What'chu mean system, Willis?
A phage virus is a virus that is made of only proteins and DNA and takes over a bacterial cell for it's own purposes.
It is the model specimen to work with in figuring out which substance (DNA or protein) makes up the genetic material because it only contains the two components.

2) What were the experimental methods that Hershey and Chase used in their experiment? How did they radioactively tag proteins? How did they radioactively tag DNA?
They "raised" strands of phage in two flasks: one containing radioactive phosphate (which DNA contains) and one containing radioactive sulfur (contained in proteins). They then injected the radioactive strands of the phage into the mice, took samples and centrifuged the results to discover what the genetic material was. Turned out to be DNA. (yayyy!)

3) What were the results of the Hershey and Chase experiment? How were they able to determine conclusively that the genetic material injected into bacterial cells by the phage virus was DNA?
OK, so to repeat myself:

  • Centrifuged the samples from inside the infected cells of the mice
  • Discovered that the genetic substance was the same radioactive color as the substance they had stained the phosphorous
  • Because of the results, they concluded that the only substance the genetic material could be was DNA.

Concept 7 – Unraveling the structure of DNA: there was key information about DNA that Watson and Crick used to come up with their model for the structure of DNA.

1) What is a nucleotide? What are the components that make up a nucleotide?

2) What are the four different kinds of bases that go into making up the nucleotides in DNA?
A, T, C. G

3) What important piece of the puzzle did the work of Erwin Chargaff add to figuring out the structure of DNA? What did Watson and Crick know as a result of Chargaff’s work?
Chargaff measured DNA within different species and found that individuals within the same species always had a certain composition of bases. He also noted that the amount of A = the amount of T; and the amount of G = the amount of C.
Watson and Crick put together that the strand of DNA was anti-parallel and uniform apart.

4) What was known about the structure of DNA based on the results of the work of Rosalind Franklin? What did she realize about DNA based on her own work? What technique did she use?
She discovered the helical structure of the DNA molecule. She used X-ray crystallography to discover this structure.

Concept 7 – Watson and Crick came up with a model of DNA that showed two strands of nucleic acids that wound around each other in a helix.

1) Where are the sugars and phosphates in this model of DNA? Where are the bases?
The sugars and phosphates are on the outside of the helical structure. The bases are on the inside.

2) By knowing from Franklin’s pictures that the DNA molecule is of uniform width, what could Watson and Crick figure out about the arrangement of bases in the molecule?
The shorter bases had to pair with the larger bases in order to keep the structure uniform.

3) What does it mean to say that the two strands of nucleic acids are “anti-parallel”?
It means that they run parallel to each other but they run opposite each other.
One strand runs 5' to 3' while the alternate strand runs from 3' to 5'. The easiest way to think about it is like magnets: the opposite primes attract.

4) What is so important about the fact that the two strands are bound to each other only by hydrogen bonds?
It means that the hydrogen bonds can easily be broken, which makes it easier for breaking apart the molecule and duplicating it.

Lecture 23 (Molecular Inheritance I) Post Lecture

Task 3: Post-lecture Assignment – One short article “Rosalind Franklin: Unraveling the Controversy and the Structure of DNA”

1) As this article states, the story about discovering the structure of DNA is a “tale of competition and intrigue.” What was the technique that Rosalind Franklin used to create pictures of DNA molecules? These pictures were shown to Watson and Crick—who showed the pictures to Watson and Crick? Were the pictures shown with Franklin’s permission?
Franklin was well-learned in the methods of X-ray crystallography, which was the process that allowed her to see the image of DNA. Wilkins was the one who showed the photograph to Watson and Crick, who realized what the image meant.

2) Who was Franklin working with when she worked on the structure of DNA? Do you think Rosalind Franklin should have been given more credit for the part she played in the discovery of the structure of DNA?
As the article says, I believe it was Wilkins who Franklin was working with; although Wilkins assumed Franklin was there merely to be an assistant and not a colleague. I think she should definitely be given more credit than she had for her work. After all, if it wasn't for her image of the DNA structure, Watson and Crick wouldn't have been able to discover what DNA looked like or even make a model of it and "discover" it.

3) When and how did Rosalind Franklin die—how old was she? When, in relation to Franklin’s death, was the Nobel Prize awarded for the discovery of the structure of DNA? Who are the three scientists who shared the Nobel Prize for this?
She died in 1958 when she was roughly 38 from Ovarian cancer. The Nobel prize was awarded to Crick, Wilkins and Watson. The prize was awarded in 1962.

Lecture 24 (Molecular Inheritance II) Pre-Lecture

This video shows three animations of DNA replication. DNA replication is a fascinating and complex process, and life depends upon it being done with few errors. Errors result in mutations, and mutations can lead to diseases such as cancer. Mutations, however, are also the basis of evolutionary change.

From watching the video, what does the enzyme helicase do during DNA replication? What does it mean to say that the process of DNA replication is semiconservative? When DNA is being replicated, what is the leading strand? What is the lagging strand? What does DNA polymerase III do? What are Okazaki fragments, and why are they produced?
Helicase splits apart the strands of DNA. The process is semi-conservative because it half conserves one strand of DNA for each new duplicated strand. The helicase splits the DNA into two strands then a new strand forms (using DNA polymerase III) and connects to one of the existing strands of DNA.

Lecture 24 (Molecular Inheritance II) Lecture

Task 2: Lecture Movie on “Molecule Basis of Inheritance - II” and Campbell Chapter 16

1) Why is it important that the replication of DNA is done accurately?
Because if it's not, it can create mutations that can mutate other cells and cause cancer, or it can have missing bases in the DNA. The missing bases (and even the mutations) are not so bad as long as they are not in a significant part of the DNA. Something like 96% of DNA doesn't code for anything, so if the mutation or missing/substituted base is in one of those areas, the DNA molecule should be fine.

2) Why does DNA replication have to be fast? Every time a human cell divides, about how many nucleotides have to be replicated?
Replication has to fast in order for it not to (for lack of a better word) fuck up the process. There are ~8 billion nucleotides that have to be replicated.

Concept 2 – Review: You have already learned that DNA is the genetic material, and you already know about the structure of DNA.

1) What specific details can you list about the structure of DNA (these are all listed in the lecture movie)? How many strands make up a DNA molecule? What does it mean to say that the two strands of DNA are antiparallel?
I love how these questions answer themselves. OK.
DNA has:

  • 4 base pairs (nucleotides): A, T, C, G
  • Has a phosphate-sugar backbone
  • It's a double helix
  • Strands are held together by hydrogen bonds
  • Nucleotides form in a 5' to 3' orientation

Two strands make up a DNA molecule. And anti-parallel means that they are parallel, but one strand runs from 5' to 3' while the other strand runs 3' to 5'.

2) What is a nucleotide? What are the different parts of a nucleotide? What are the four different bases that go into making the four different nucleotides of DNA? What base does adenine pair with? What base does guanine pair with?
Nucleotides make up the structure of DNA. Nucleotides are composed of the base (A,T,C,G). "Guanine met cytosine and fell in love / and thymine got busy with adenine."

Concept 3 – There are several models of DNA replication: the conservative model, the semiconservative model, and the dispersive model. The results of an experiment by Meselson and Stahl showed that the semiconservative model for DNA replication is the accurate model.

1) What does each model named above propose as a method of DNA replication?

  • Conservative Model: one strand of DNA replicates and creates a new duplicated strand of that DNA and the original strand. In the third replication, there are three new(er) replicated strands of DNA and one original strand.
  • Semi-conservative Model:You have one strand of DNA which breaks apart and each strand of the original gets copied and put together with a new strand of DNA.
  • Dispersive Model: DNA is all chopped up into fragments (the original and the new) so that the DNA is a complete combination of both.

2) What organism did Meselson and Stahl use in their experiment to test how DNA replicates? Why was this a good organism to use for these experiments?
They used bacteria (I don't remember if it was specified which one….but Wikipedia says //E. coli]. This was a good organism to use because bacteria have a relatively small amount of DNA and they replicate quickly.

3) What methods did Meselson and Stahl use in their experiment? How did they tag DNA molecules?
They realized that the structure of the bases contained N where the other parts of DNA did not. They used two isotopes of Nitrogen: 14N and 15N. The 15N isotope had a higher density and was easier to "tag". They allowed bacteria to grow and flourish in the 15N solution and, after several replications of DNA, they transferred the bacteria from the 15N flask to the 14N.

4) In this experiment, after one round of replication, what results did Meselson and Stahl get? What model did these results disprove?
One round of replication, there was a single band of 15N, which disproved the Conservative Model (because that model predicted there would also be a 14N band because one new strand is appears alongside the original in duplication).

5) After two rounds of replication, what results did Meselson and Stahl get? How did these results support the semiconservative model? How did it disprove the dispersive model?
They saw two bands: one of the less dense N sample and one of the more dense. Wikipedia answers the last part of the question nicely: "This was inconsistent with dispersive replication, which would have resulted in a single density, lower than the intermediate density of the one-generation cells, but still higher than cells grown only in 14N DNA medium, as the original 15N DNA would have been split evenly among all DNA strands."

Concept 4 – During DNA replication, both strands of DNA are replicated simultaneously! This is an amazing feat, considering that replication occurs in the 5’ to 3’ direction, exclusively.

1) What is the first step in replication—i.e., what has to happen to the double stranded helix before any replication can occur?
The helicase needs to come in and split apart the bonds by dispersing of the hydrogen bonds holding the strands together.

2) What does it mean to say that DNA replication occurs in a 5’ to 3’ direction? What marks the 5’ end of the DNA strand? The 3’ end? When a new nucleotide is added, what is it attaching to on the nucleotide just before it?
It means that DNA replication only happens from 5' to 3' (how does that not make sense?) An RNA primer (left by the enzyme primase) attaches to the end of the 5' strand. At the end of the 3' strand is DNA ligase.

3) What does it mean to say that the original DNA strands are used as the templates for the new strands, i.e., how is the template strand being use to guide the making of the new strand?
The bases have to match. Adenine can not pair with cytosine. It doesn't work. So the original strand of DNA would be the "blue print" for the new strand, where the DNA polymerase III can add the required bases.

Concept 5 – When DNA replication begins, it starts at an origin of replication. Prokaryotes such as bacteria have a single circular chromosome with one origin of replication. In eukaryotic cells, the chromosomes are linear and have many origins of replication.

1) Why do you think a bacterial chromosome has only one origin or replication, when our chromosomes have many?
The bacterial genome is significantly smaller than ours.

2) Why do you think our chromosomes (and those of eukaryotes in general) have many origins of replication on each chromosome?
Because our DNA is larger and it all needs to happen simulataneously.

3) What is a replication bubble? What is a replication fork?
A replication bubble is
A replication fork is the start of replication, where the helicase begins to break down the hydrogen bonds between the strands.

4) Can you see a replication bubble using your light microscope in lab? What type of microscope would you have to use in order to see the replication bubble in a chromosome?

Concept 6 – For DNA replication to take place, you need DNA (of course), the substrates (nucleotides) to build the new strands of DNA, a bunch of enzymes to do the work of assembling the new DNA strands, and chemical energy to provide the energy for polymerization of the new strands.

1) How many different kinds of nucleotides are there for building the new DNA strands?
How many different kinds? Uhm…four?

2) What enzyme is used to polymerize the new strands of DNA?
DNA polymerase III

3) Where does the chemical energy come from for the polymerization of the new strands of DNA?
It comes from within the nucleotides themselves and resembles ATP (I think they said it was called dATP but check on that!)

Concept 7– DNA polymerase III is the enzyme that polymerizes the new strands of DNA. It can only work in a 5’ to 3’ direction. It cannot start making new DNA without a primer.

1) What is a primer? What is it made out of? What is it attaching to? Why does DNA polymerase III need a primer to start making new DNA?
A primer is used as the starting point of DNA synthesis. Primers are made out of _. It is attaching to the 3' end of the DNA strand. DNA Polymerase III needs the primer because DNA runs in the 5' to 3' direction, but DNA Poly. III cannot synthesize 3' to 5'.

2) How does DNA polymerase use the template strand as it is making the new strand of DNA?
DNA Polymerase III uses the parental DNA as a template to synthesize a new DNA strand by covalently adding nucleotides to the 3' end of a pre-existing DNA strand or RNA primer.

3) How are the primers eventually removed from the new DNA strands? How is DNA polymerase I involved in this process?
Primers are removed by DNA polymerase I and are replaced with DNA nucleotides.

Concept 8 – When the new strands of DNA are made, one strand (the leading strand) is a long molecule of DNA, the other strand is a series of small fragments of DNA called Okazaki fragments.

1) During DNA replication, why can’t the DNA polymerase simply make two long strands of DNA – why instead is one of the new strands made up of short segments (the Okazaki fragments)?
Because the lagging strand goes in the 5' to 3' direction and DNA can't be synthesized that way. So it is split into fragments to be easier synthesized.

2) How are the Okazaki fragments finally stitched together? Does this occur before or after the primers are removed?
DNA ligase stitches the Okazaki fragments together. This occurs after the primers are removed.

Concept 9 – DNA replication is incredibly accurate, with fewer than one error per 10 billion bases. But the DNA polymerase, itself, isn’t as accurate and makes an error every 100,000 bases.

1) How are errors in DNA repaired? What enzyme is able to proofread the new DNA as it is being made? How does it recognize a mismatch? What is mismatch repair?
DNA polymerase I repairs the DNA as it moves along the strand and is incredibly accurate. I don't know how it recognizes it but when it does, it removes the wrong nucleotide and replaces it with the right one.

2) What external agents can cause errors in DNA? Are you exposed to any of these agents on a daily basis?
X-rays, UV radiation, cancer-causing agents, etc.

3) What is excision repair?
Excision repair is what happens when an error happens after replication. In this process, the repair mechanisms come in, take out the wrong chunk of DNA and replaces it with the appropriate chunk.

Lecture 24 (Molecular Inheritance II) Post-Lecture

1) As this article states, X-rays cause mutations by damaging DNA. What kind of damage do X-rays cause in DNA?
They create mutations and make substitutions in the code. I am doubtful about this, though, because although it is true that radiation does cause cancer and there is an increased risk to having X-rays done….mutations in the DNA happen and they are very rare, but they do happen. And if 96-98% of the code doesn't actually code for anything…how is it bad? I am just wondering where the data comes from because they did happen to blame a very higher rate of radiation-related cancer on those in Japan…WHO WERE HIT WITH TWO NUCLEAR BOMBS SEVENTY YEARS AGO. Radiation still persists. ><

2) Since DNA damage leads to mutations, and this can lead to cancer, is it at all surprising that X-rays can cause cancer! And yet X-rays are often used for medical purposes. Do CT scans use more or less X-rays than a standard chest X-ray? The article discusses a paper published in The Lancet. In this paper, how many cases of cancer do the authors estimate are caused each year by X-rays from medical imaging devises?
Well, I don't know about CT scans because the article didn't mention that.
18,500 cases of cancer/year in 15 countries studied (including Japan. Because these people are biased, or just dumb. I don't know).

3) What are your own conclusions from this study?
I'm unsure. This isn't a study, this article. It's a blurb. Besides, there is no data to show how they tested for their results, there is no overview of their results. The way the article is written, it sounds more like they assumed the data, or something. Maybe I am just being a biased bitch. Who knows. But it's unsure where the data came from; if the American data or UK data came from a certain area or they took an average or took a compilation over the entire area….or if they had any radiation in the past (which they obviously didn't do because they made a comment at the extreme high levels of radiation in Japan).

Lecture 25 (Transcription) Pre-Lecture

Task 1: Pre-lecture Introduction –Video “DNA Transcription and Protein Assembly”

This video has two different segments showing animations of DNA transcription in a eukaryotic cell. The first segment also includes the translation of mRNA into protein. The first segment is oversimplified, but is gives you a nice review of the entire process. The second segment is more detailed in its portrayal of how mRNA is made.

1) From seeing these videos, how would you define transcription? Where is transcription taking place—in the nucleus or cytoplasm? In the first segment, what is the “machine” that the video shows transcribing DNA into RNA? Once the RNA is made, this first segment skips over a whole chunk of stuff that happens before the RNA transcript can leave the nucleus as mRNA. What are some of the steps that the movie leaves out? (Hint: the second segment shows these nicely.)
Transcription is the process of transforming RNA from segments of DNA in order to send the ribosomes in order to create proteins. The transcription is taking place in the nucleus. I don't know what the parts are that the movie leaves out. I don't read the text and I don't pay enough attention in BMB to know. But I am assuming I will know this later on. So….yeah.

2) The first segment also talks about translation. How would you define translation? Where in the cell does translation occur—in the nucleus or cytoplasm? What structures does the mRNA dock onto for translation? What is the mRNA being translated into?
How would I define translation? Well, let's have a better one. How does Wikipedia define it? "Translation is the first stage of protein biosynthesis (part of the overall process of gene expression). 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. Translation occurs in the cell's cytoplasm, where the large and small subunits of the ribosome are located, and bind to the mRNA." mRNA translates into a protein.

3) The second segment reviews the processing of RNA within the nucleus. What are three things that have to happen to the RNA transcript before it can leave the nucleus as mRNA?

  • Machine unwinds the DNA strand to expose a certain segment for protein synthesis.
  • Another machine comes through and copies these instructions to form a strand of mRNA.


Lecture 25 (Transcription) Lecture

Concept 1 – Genes from one organism can be inserted into completely different organisms and be expressed! The genetic code is universal!

1) What examples are shown to illustrate that the genetic code is universal, i.e., that every organism can read the same genetic code?
The main example is of the fluorescent pig. They took genes from a luminescent green jellyfish and inserted them into the pig.

2) The gene for green fluorescent protein has become a very powerful tool in biological studies. What organism does it come from? If you put this gene into a pig embryo, when that pig grows up, will that gene for green fluorescent protein be expressed? How would you be able to tell?
Jellyfish. Yes. The damn pig is green.

Concept 2 – Transcription is just the first step in going from a gene to a protein. In transcription, the
information stored in DNA is converted into RNA.

1) To go from a genotype to a phenotype, what are the two different processes that must occur? Where do each of these occur in a prokaryotic cell? Where do they occur in a eukaryotic cell?
Transcription and translation. They occur in the cytoplasm of prokaryotic cells and in the nucleus of eukaryotes.

2) Bacteria do not sequester transcription within a nucleus, but eukaryotic cells do. Do you see any advantages to the system in bacteria? Can you think of any advantages to the eukaryotic system, i.e., having a physical barrier (the nuclear membrane) between the machinery of transcription in the nucleus and the machinery of translation out in the cytoplasm? Explain your thinking.

Concept 3 – The results of an experiment by Beadle and Tatum indicated that each gene codes for a single protein. By studying mutants of the bread mold, Neurospora crassa, they showed that when they mutated one gene, they knocked out a single enzyme. When they mutated a different gene, they knocked out a different enzyme. And when they mutated a third gene, they knocked out yet a third enzyme. From this they proposed that one gene codes for one enzyme: the one gene-one enzyme hypothesis.

1) What were the methods that Beadle and Tatum used? How did they create mutants of the bread mold? What specific mutants did they then select for? How did they select for these mutants?
They chose their model organism. They grew the mold in a minimal medium (MM). They used radiation (in this case, a form of X-ray). They selected for mutants that would only grow if introduced to arginine. They selected for these mutants by looking for the bacteria that would only grow if introduced to arginine.

2) From what we know now, what is wrong with the one gene-one enzyme hypothesis? If we were to state it as one gene one polypeptide, would it be more correct? Why? What is a polypeptide? Can an enzyme or any protein be made up of more than one polypeptide chain?
Because not all genes code specifically for one enzyme. Yes. Because the movie said so. A polypeptide are short polymers formed from the linking of alpha-animo acids. Wikipedia

Concept 4 – To go from DNA to protein, first DNA is transcribed into RNA, and then RNA is translated into protein. This occurs in all cells in all domains (bacteria, archaea, and eukaryotes).

1) Why is the conversion of DNA into RNA called transcription? How do the nucleotides of DNA differ from the nucleotides of RNA?
Because the DNA strand is rewritten into RNA. Thymine is not thymine in RNA; it is uracil.

2) Why is the conversion of RNA into protein called translation? What are the subunits called that make up a protein?
It's called translation because it's being translated into another nucleic strand (from deoxyribose to ribose).

3) How does transcription in a bacterium differ from transcription in a eukaryotic cell?
mRNA in a prokaryotic cell doesn't go through the re-mRNA stage.
There are also three things that only happen to eukaryotes:

  • something is going to happen to the 5' end (the addition of a backwards guanine nucleotide)
  • something is going to happen to the 3' end (the addition of an Poly-A tail)
  • between the two strands, chunks will be removed.

Concept 5 – Transcription can be divided into three steps: initiation when transcription begins, elongation when the RNA molecule is made, and termination when the RNA stops being made.

1) How is RNA polymerase involved in transcription? What does it do? Can more than one RNA polymerase be transcribing a gene at the same time?
RNA polymerase is the enzyme that makes transcription happen, really. It opens up the two strands of DNA and inserts complimentary ribonucleotide bases to create an RNA strand. I don't know about the "more than one at time" thing.

2) What is a transcription unit? What are the different parts of a transcription unit?
A transcription unit tells the RNA polymerase where to start and where to stop transcribing.
Well, there are three steps:

  • initiation
  • elongation
  • termination

3) What happens during the initiation step? How is RNA polymerase involved?
RNA polymerase starts the transcription process by:

  • unwinding a small section of DNA
  • picking a section it is going to copy for
  • start inserting ribonucleotides to compliments the deoxyribonucleotides.

4) What happens during the elongation step? How is RNA polymerase involved?
The RNA polymerase will keep adding nucleotides all along the gene until it hits the stop codon.

5) What happens at the termination step? How is RNA polymerase involved?
The polymerase will fall off and the RNA transcript will be complete and detach from the strand of DNA.

6) What has been made during this process? In a eukaryotic cell, why is it called a pre-messenger RNA?
An mRNA strand has been made. I believe that pre-mRNA is simply the final mRNA strand without the last three steps (mentioned above) having yet taken place.

7) In making the RNA, which end of the RNA is made first, the 5’ end or the 3’ end?
the 5' end.

8) If a stretch of DNA being transcribed had the following nucleotides—T,A,G,G, T, T, A, A, C, C—what nucleotides would the corresponding RNA molecule be made up of? (List them in order.)

Concept 6 – A promoter is a region of the gene where the RNA polymerase attaches—the promoter helps the RNA polymerase find the start point. Transcription factors are proteins that bind to the promoter region, allowing the RNA polymerase to attach; the RNA polymerase cannot attach without the help of the transcription factors. There are many different transcription factors, and they are specific for specific genes.

1) What specific region indicates a promoter region in a gene in eukaryotic cells? Why is it called a TATA box?
The 5' end? (I don't know if it's cuz I'm tired or not but that section of the question doesn't make much sense…). Or maybe she just means the answer's the TATA box because of how the question is worded.
The TATA box tells the transcription factors where to bind.

2) What is the function of transcription factors? Why have them at all?
The job of transcription factors is to keep all the genes we have in our genetic code from being expressed at all times.

3) Why is it important to have different transcription factors that are specific for specific genes?
Because it makes the system more efficient and effective. You don't want a transcription factor that works with heat exhaustion to be on a gene that's for hunger pains. That would be a little confusing. :/

Concept 7– In eukaryotic cells, the RNA that is transcribed is called pre-messenger RNA; pre-messenger RNA has to be processed before it can leave the nucleus as messenger RNA (mRNA).

1) What three things happen to pre-messenger RNA to make it into mRNA?

  • something is going to happen to the 5' end (the addition of a backwards guanine nucleotide)
  • something is going to happen to the 3' end (the addition of an Poly-A tail)
  • between the two strands, chunks will be removed.

2) What is the 5’ cap? What is the function of the 5’ cap? What is the poly-A tail? What is the function of the poly-A tail? On which end of the mRNA is the poly-A tail, the 5’ end or the 3’ end?
The 5' cap is made up of a backwards guanine nucleotide. It works to protect the end from degredation. A poly-A tail is made up of a long string of adenine nucleotides. It also protects but it also allowes the mRNA to leave the nucleus.

3) What is an intron? What is an exon? What happens to the introns? What happens to the exons?
An intron is an "intervening sequence" and they don't get translated into proteins. Exons are "expressed sequences" and do get translated into a polypeptide.

4) What are some possible reasons for having introns?
To create a more diversity in protein structure.

5) How can a messenger RNA be alternatively spliced to give different mRNAs?
Using introns.

6) How can one gene code for more than one polypeptide?
Using introns.

Lecture 25 (Transcription) Post-Lecture

Task 3: Post-lecture Assignment – One short article “Alternative Splicing and Disease”

1) This article talks about the alternative splicing of RNA to form different mRNAs. From reading the article, what percentage of human genes are thought to produce transcripts that are alternatively spliced? Now that we know about alternative splicing, do we have to give up the dogma “one gene, one polypeptide”? How should we rephrase this to be more accurate?
The article says that about 80% of genes are alternatively spliced. We could say "one gene-n polypeptides". Or "one gene-many polypeptides". Or "one gene/ there-may-be-more-we-don't-really-know-yet-but-be-aware polypeptide(s)". Or just come up with an equation for one gene has x number of polypeptides (which is the same example I gave above with the whole "n polypeptide" business, but now I am just being obnoxious).

2) Can mutations that affect alternative splicing cause disease? What are some examples that indicate mutations that result in abnormally spliced mRNAs can lead to cancer?
There is evidence of more mRNA mis-spliced strands are found in cancerous tumor cells than in normal cells. So……there could be a correlation there.

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