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18 Nov 2018

Suppose that you compare the levels of nonsynonymous and synonymous substitutions (i.e. you perform the kA/kS test) on a particular coding region of a gene. You find that kA/kS = 0.3.

(a) What type of selection, if any, would this result support?

(b) You also examine levels of polymorphism around this particular gene in a sample of 20 individuals from the population of interest. You find that Tajima’s D is -2.8. What type of selection, if any, would this result support?

(c) Provide 2 explanations for why the kA/kS test and the Tajima’s D test appear to give contradictory results.

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Patrina Schowalter
Patrina SchowalterLv2
19 Nov 2018

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1. A) Explain how changes in the environment drive evolutionary change. B) Provide and explain an example

2. A) Explain how the Hardy-Weinberg equation allows us to find evidence of evolution. B) Could processes other than Natural Selection result in deviation from the Hardy-Weinberg equilibrium? List and explain each one: C) define what the process is and D) the effect it has on the allele frequency.

3. A gene that is responsible for multiple traits (pleiotropy), for example the same allele causes sickle-cell anemia and provides resistance to malaria. Would a gene that controls these two traits respond equally to natural selection favoring malaria resistance as a non-pleitropic gene that only controls malaria resistance? Explain your answer.

4. A) Explain how lack of genetic variation limits evolution and provide an example. B) Explain how epistasis limits evolution and provide an example

Questions 5-6 are based on the following:

Let’s say you are studying a population of Japanese four o’clock plants. In these plants, the allele for red color flower shows incomplete dominance over the allele for white flowers. This is very convenient for this experiment because you can distinguish the heterozygous (pink flowers) from the homozygous dominant (red flowers). For your experiment, you produced a large number of plants, 25% had red flowers, 25% had white flowers and 50% had pink flowers. You transplanted them into different habitats and left some in the lab (using the same proportions in all the habitats). You waited a few years, while plants reproduce for a few generations and then you go back and resample the populations you’ve transplanted.

5. In the lab you ensured that all individuals receive all requirements to grow and reproduce and mate randomly. A) What do you expect the distribution of the phenotypes after a few generations breeding in the lab? B) Is the lab population in Hardy-Weinberg equilibrium? Yes/No, explain

6. In habitat A, you find that you only have red flowering plants and white flowering plants but there are no pink flowering plants. A) Is the population in habitat A in Hardy-Weinberg equilibrium? Yes/No, explain. B) Which one(s) of the five agents of evolutionary change could be responsible for these results? Explain. C) What type(s) of selection (stabilizing, disruptive, directional, oscillating, etc...) could be responsible for the results in habitat A? Explain

If you are able to answer any or all of these that would begreat!!!

25. Talked about the warburg effect ( aerobic glycolysis) inwhich cancer cells preferentially use fermentation instead of goingthrough oxidative phosphorylation. Answer the followingquestions?

A) If cells are going to preferentially use fermentation, theyneed to transport higher levels of glucose into the cell. Explainwhy this is so?

B) Cells that preferentially use fermentation had higher levelsof the GLUT1 carrier protein at the membrane. explain the mechanismGLUT1 uses to bring glucose into the cancer cells?

C) If the GLUT1 transporter is composed of two main domains,what are their likely functions? what is the nature of the aminoacids within each domain?

D) What are two ways cells could increase the amount of GLUT1transporter on the cell membrane? Briefly explain each.

E) What is the one way the rate of movement of glucose into thecell through GLUT1 carriers could be altered ( either increase ordecreasd)? Describe a change you could make and be sure to indicatehow it would alter the rate of glucose uptake( either increase ordecrease)?

F) A drug called fasentin inhibits GLUT1 carriers. However, whenyou treat FTC133 cells with fasentin, they do not die. What is onehypothesis for how they are surviving in the absence ofglucose?

G What is a prediction that you could make based on yourhypothesis?

H) In the paper, the authors conclude that adding the PTEN backinto the cancer cells via transfection decreases the amount ofglucose that FTC133 cells take up. You hypothesize that HeLa cellsmight benefit from having additional PTEN protein. YOu transfectDNA coding for the PTEN protein into the HeLa cells and perform awestern blot to confirm PTEN expression. Unfortunately, you do notsee any expression of PTEN. What is one possible reason you dontget PTEN expression in your HeLa cells? ( HINT: you know yourantibodies are working and that transfection was successful, sothink about factors controlling gene expression)

I, Since you couldnt get PTEN expressions in the HeLa cells, youdecide to return to the FTC133 cells in order to test if the lipidphosphatase activity of PTEN is required for its ability todecrease glucose consumption. What type of mutation ( silent,missense, nonsense? frameshift or not?) would you introduce intothe PTEN gene in order to destroy the catalytic ability of PTENprotein while retaining the rest of the protein's structure andfunction? Explain your answer.

J) Next, you decide that you want to purify large amounts ofyour wild type and mutant PTEN proteins to test their catalyticabilities in in vitro. Your labmate suggests that you transform (insert) your DNA into bacterial cells because they are rapidlygrowing and are know to express large amounts of protein under theright conditions. You consider this but are unsure as to how wellyour human PTEN protein might be expressed in these cells. Based onwhat you know about the genetic code and about gene expression inprokaryotic and eukaryotic cells describe (i) one reason why yourgene might be able to be expressed in bacterial cells under theright conditions and (ii) two reasons why your PTEN gene might notbe expressed properly. (iii) Then, decribe one modification thatcould be made to your PTEN DNA to increase the likelihood that itwill be expresssed in the bacteria.

Homozygous recessive loss of function mutations in any one of 4 different genes in C. elegans worms (genes A, B, C, or D) results in female worms that don't form proper egg-laying structures, called vulvas, as shown in Lines 2-5 of the data table below. In vulvaless females, the fertilized eggs hatch and baby worms develop inside the mother, killing her in the process.

genotype phenotype
1 AA BB CC DD (wild type) normal vulva
2 aa BB CC DD No vulva
3 AA bb CC DD no vulva
4 AA BB cc DD no vulva
5 AA BB CC dd no vulva

You would like to figure out the order in which these genes act during the creation of the vulva (you cannot assume it will be A--->B--->C--->D as the gene names are arbitrary). Your friend tells you to perform epistasis analysis by making double mutants between the different homozygous recessive mutants and analyzing the phenotype of the double mutant. For example, she asks you to examine the phenotype of aabbCCDD (double mutant of genes A and B) and compare this to the single mutants to figure out whether gene A acts earlier than gene B, or vice versa. You know this won't work. Why not? Pick the ONE BEST choice:

a. The phenotype of the single mutant is already pretty severe. The double mutant will most likely be dead, therefore epistasis analysis won't be possible.

b. Each of the single mutants (aaBBCCDD) and (AAbbCCDD) has the same mutant phenotype i.e., no vulva. Epistasis analysis between any 2 genes is only possible when the mutant phenotypes for each gene is different.

c. Epistasis analysis involves making triple mutants (such as aabbccDD) in order to learn something about how the genes are ordered.

d. Epistasis analysis can never be carried out with null loss of function mutations. The mutations being analyzed all have to be dominant gain of function alleles.

To address your concern, you first generate overactive alleles of either gene A (denoted as A*) or gene B (denoted as B*). As shown in lines 6-7 of the table below, C. elegans that have one of these overactive alleles produce multiple vulvas.

Genotype Phenotype
6 A*A BB CC DD multiple vulvas
7 AA B*B CC DD multiple vulvas

To find out the order in which these genes act, you combine the overactive alleles with different loss of function alleles and observe the phenotype in double mutants (see Lines 8-11).

Genotype Phenotype
8 A*A bb CC DD multiple vulvas
9 A*A BB cc DD multiple vulvas
10 A*A BB CC dd no vulva
11 AA B*B cc DD multiple vulvas

Based on the data in the table, what is the order in which these 4 genes normally act in wild-type C. elegans in order to produce a wild-type/normal vulva?

a. A----> B----->C----->D ---> Vulva

b. D----> B----->C----->A----> Vulva

c. B----> C----->A----->D----> Vulva

d. C----> B----->A----->D----> Vulva

e. C----> B----->D----->A----> Vulva

f. don't have enough data to make any conclusions

Based on the vulva formation phenotype of the double mutants, which of the following statement(s) accurately describes the genetic interactions between the A* allele and alleles of other genes affecting vulva formation? Pick ALL that apply:

a. The A* allele is epistatic to homozygous recessive loss of function mutations in gene B

b. A homozygous recessive loss of function mutation in gene B is epistatic to the A* allele

c. Homozygous recessive loss of function mutation in gene D is epistatic to the A* allele

d. The A* allele is epistatic to homozygous recessive loss of function mutation in gene D

e. The A* allele enhances the homozygous recessive loss of function mutation in gene D

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