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Azaserine is a structural analog of glutamine. It is a competitive inhibitor of many enzymes that use glutamine as substrates. What three biosynthetic products would you expect to be inhibited by azaserine. Do you think that eating azaserine would be immediately fatal? Why or why not?

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Nelly Stracke
Nelly StrackeLv2
2 Jan 2018
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Related questions

You isolate 3 new yeast mutants (mutants 1, 2, and 3) that are not able to grow unless the amino acid glutamine is added to the growth medium. Genetic analysis tells you the mutants are defective for different genes. You first analyze the mutants for glutamine synthetase (GS) enzyme activity, and all three have undetectable levels of it. Mutant 1 makes normal levels of GS mRNA and protein and the protein is normal in size, while mutants 2 and 3 do not make GS mRNA or protein. You next analyze levels of histone acetylation at the glutamine synthetase gene promoter, and find that they are normal in mutant 1 and mutant 3, but low in mutant 2. Finally, you do a DNAseI hypersensitivity assay and find that mutant 1 looks the same as the wild type, but mutants 2 and 3 have lost a hypersensitive site that is present near the promoter of the GS gene in the wild type.

a. If the mutations causing the 3 GS gene defects are in a chromatin “writer” gene, a chromatin “reader” gene, and in the GS gene, which mutant is defective for which gene? Explain your answers.

Mutant 1:

Mutant 2:

Mutant 3 :

b. For the GS gene mutant, indicate where in the GS gene the mutation must be (promoter, enhancer, splice junction, coding region missense, coding region nonsense) and explain why.

c. For the chromatin writer mutant, name the enzymatic activity it must encode, and explain why. d. For the chromatin reader mutant, name the complex or complexes that could be affected, and explain how you know this.

Stimulation of de novo pyrimidine synthesis by growth signaling

through mTOR and S6K1, Ben-Sahra ET AL, Science 2013

1.How does mTORC1 affect lipid and sterol synthesis?

2. How is mTORC1 activated?

3.What 5 metabolites decrease in response to treatment of cells with rapamycin?

4. What pathway had significant in metabolic flux in Tsc2 -/-cells?

5. Describe the data that shows the affect on Tsc-/- cells of long-term sensitivity to rapamycin by the formation of carbamoyl-aspartate. Explain how these findings were confirmed?

6. Explain the results showing that glutamine flux was not affected by rapamycin. From you knowledge of glutamine synthesis and utilization, what is the reason for it not might not being controlled in these transformed cells? Hint think glutamine utilization as a source of αKG.

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8. What does the CAD transcription and expression data show about the affect of mTORC1 on CAD?

9. Insulin stimulates the phosphorylation of CAD. Discuss the data and what does this show about control of this pathway?

10. Analyze the data of Figure 4. What do these results indicate?

You are a researcher looking at different ways you can utilize plants’ ability to make its own glucose and replicate it outside of a plant cell. You start by isolating mesophyll cells from the three types of plants: C3, C4, and CAM plants. You want to predict what will happen to the outputs of photosynthesis by changing the different concentration of the inputs to each type of plant.

You add a poison that acts as an inhibitor that binds to Rubisco but you don’t know what type of inhibitor that it might be.

a) Describe two types of inhibitors that would be involved.

b) What type of experiments could you conduct to discriminate between the two? Explain your experiments.

c) Could Rubisco also be inhibited by allosteric inhibition? Explain how would this work or would not work.

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