When a monohybrid heterozygote is test crossed, the following phenotypes are produced:

Phenotype I = 213

Phenotype II = 87

Determine if this cross follows Mendelian rules of segregation. Be careful to state your hypothesis and conclusion, degrees of freedom, and p value (range is ok), and SHOW YOUR WORK.

What are the major similarities and differences between DNA repair in prokaryotes versus eukaryotes?

Genetic Code:

Using the standard genetic code, write a sequence encoding the peptide "MASTERMIX"

How many different sequences can encode this peptide?

How many genetic codes have been described? (Hint: search NCBI Genetic Codes)

How, in a general way, do these alternative codes tend to differ from the standard genetic code?

How is selenocysteine encoded?

1. In presenting the parts of the scientific method, give an example of how people use the scientific method in everyday life. One example may be the use of premium versus regular gasoline. You can propose conditions which should remain constant as well as the type of mathematical data that could be collected and analyzed

The demand for farming is increasing, which is destroying native forests and affecting their biodiversity.

1. what is the issue?

2. background information?

3. restoration method? two examples?

4. why is this the best method?

5. end goal for the project?

6. subgoals?

7. time frame?

PLEASE be descriptive and in depth with these responses so I can fully understand the content, at least more than 20-30 word responses

Briefly describe how protein and lipid metabolism are linked to glycolysis and the Krebs cycle, and determine the ATP yield of each.

how does mitochondria get oxygen in anaerobic conditions?

1. Which is the mRNA complement of the DNA sequence 5’ ACGGTCGGAT 3’

1. 5’ ACGGTCGGAT 3’
2. 5’ AUCCGACCGU 3’
3. 5’ TGCCAGCCTA 3’
4. 5’ UGCCAGCCUA 3’

2. Answer question a in the first row (with a number).

For statements b-k, enter an X to indicate if it is associated with DNA replication, transcription or translation. A statement may apply to more than one.

3. The start codon to begin translation is 5’ AUG 3’. Which of the following is the complementary DNA sequence on the template strand?

1. 3’ AUG 5’
2. 3’ TAC 5’
3. 5’ AUG 3’
4. 5’ ATG 3’
5. 5’ TAC 3’

4. Examine this segment of double stranded DNA. Which is the template strand for transcription?

Strand 1: 5’ A T C T C C T G C C C C T C A T A A 3’

Strand 2: 3’ T A G A G G A C G G G G A G T A T T 5’

5. What molecule is produced through the process of transcription?

6. What molecule is produced through the process of translation?

7,Translate the following mRNA strand using the codon chart below:

mRNA:           5’ C C A U G U C C C A A C G U C C C G G A A A C U A A 3’

peptide:

4. In your studies with mice, you have sequenced a piece of wild-type DNA and it clearly contains a gene, but you do not know what this gene does. Therefore, to investigate further, you would like to create a transgenic mouse to learn more about the phenotypic qualities this gene confers. What kind of transgenic mouse would allow you to correctly determine any phenotypes that depend on this gene’s function? How would you go about making such a mouse?

The partial pressure of oxygen in the lung alveoli is a bit lower than in ambient air, being about 100 mm of mercury, or 0.13 Atm (it is lower than the partial pressure in air mainly because oxygen is continually taken up by the alveolar capillaries and carbon dioxide is continually released into the alveoli).  In cell-free blood plasma (or a saline solution formulated to match key characteristics of blood plasma), which lacks red blood cells and therefore lacks hemoglobin, the concentration of oxygen will equilibrate at 37° C at about 0.3 ml O₂/100 ml plasma. For whole blood (with hemoglobin), however, the O₂ concentration is around 20 ml O₂/100 ml whole blood.

By what factor does the presence of hemoglobin increase the oxygen content of blood?

B.  Given the above, imagine that you are an emergency room physician treating a patient who lost a quarter of his blood in an accident. A paramedic replaced this lost blood with saline solution to keep his blood pressure up. The saline solution contains no hemoglobin since it contains no red blood cells. The patient is short of breath and oxygen levels in his blood are dangerously low. If for some reason you must choose between administering pure (100%) oxygen or giving a transfusion of whole blood to restore the red blood cell count, which would you expect to be more helpful? Address this decision by answering the questions below. Show your work and be as quantitatively explicit as possible.

1. Under normal conditions, what percentage of blood oxygen content is accounted for by oxygen dissolved in the plasma and what percentage is bound to hemoglobin? By how much do these percentages change after the patient has a quarter of his blood volume replaced with saline solution?
2. a) By what percentage could total blood oxygen content be increased by delivering pure (100%) oxygen instead of allowing the patient to simply breathe ambient air? Assume that Henry’s Law applies.

b) One obviously can’t deliver oxygen at a concentration higher than 100%, but how else might the partial pressure of the oxygen being delivered be modified to increase the amount diffusing into the blood?

3. By what percentage could blood oxygen content be increased by transfusing whole blood to restore the red blood cell count? Relative to delivering pure oxygen, is this a more promising or less promising approach for restoring normal blood oxygen levels? Explain.

Taxol is a drug used in chemotherapy that interrupts the function of the mitotic spindle and prevents chromosomes from aligning properly. A cell treated with Taxol would:

A) arrest at the G1 checkpoint B) arrest at the S phase checkpoint C) arrest at the G2 checkpoint D) arrest at the M phase checkpoint E) go into the ‘resting’ G0 phase

Which of the following would you predict to find in an individual after 15 years of persistent opioid use? A) Increased gene expression of the gene encoding the dopamine re-uptake receptor protein, leading to higher amounts of dopamine in the synapse B) Reduced gene expression of the gene encoding the dopamine re-uptake receptor protein, leading to fewer dopamine re-uptake receptors in pre-synaptic neurons C) Increased gene expression of the gene encoding the dopamine receptor protein, leading to higher dopamine receptor levels in post-synaptic neurons D) Decreased gene expression of the gene encoding the dopamine receptor protein, leading to fewer dopamine receptor levels in post-synaptic neurons E) Reduced gene expression of the gene encoding dopamine

Super enhancers have been shown to regulate the expression of oncogenes like Myc. These super enhancers can be targeted by small molecule inhibitors to histone readers like BRD4. Inhibiting histone readers like BRD4 has been leveraged as a therapeutic strategy to repress oncogene expression (i.e. Myc) in specific tumor types. Can you further explain the rationale behind this approach by addressing the following questions? A.) Does BRD4 occupy super enhancers to a different extent than regular enhancers? If so, why does BRD4 bind to super enhancers differently? B.) Would BRD4 inhibition affect normal enhancers in the patient’s body to the same extent as the active super enhancers in the patient’s tumor? If yes or no why? C.) Would BRD4 inhibition in tumors of different origin (lymphoma vs neuroblastoma) affect the expression of the same oncogenes? If yes or no why?

Question 1:

1. You have been studying various oncogenes and tumor suppressor genes in tumor cell lines in vitro, but would now like to address certain questions in mouse models in vivo. For each of the questions below, briefly describe the type of mouse model you would use.
   • For xenograft/allograft experiments, briefly describe the type of cell lines you might use and the experimental end points you would be looking at.
   • For GEMs, briefly describe the type of mouse you would make (you don’t need to go into details about how the mouse is generated), and the experimental end points you would be looking at.

Note: there is no single right answer. However, try to select the model that would be most straight-forward way to initially address your question.

3. You are studying a (hypothetical) newly-described member of a family of protein kinases (XYK6), which you suspect may function as an oncogene, based upon the observation that specific point mutations (especially Thr489Asp) are sometimes seen in human breast tumors.You’ve queried the TCGA database and found that this mutation, when present, seems to be an “early” mutation, since it is seen as frequently in early-stage lesions as in later-stage tumors.You therefore hypothesize that it may be a driver mutation that contributes to the process of breast cancer initiation.Describe a mouse model that would allow you to test this hypothesis.
4. Oncogenic mutations of the (hypothetical) PRO gene are present in many tumor types, and are associated with high rates of tumor cell proliferation. Several drug companies are therefore trying to develop agents that specifically inhibit the mutant PRO gene product without affecting the normal protein. One company has approached you to assist with in vivo studies to test the efficacy of this agent and its specificity for tumors with PRO mutations. What type of mouse model would you propose to use?