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25 Dec 2018

Make a table or drawing and explain the different regulation mechanisms.

- Regulation by chromatin.
- Epigenetic regulation
- Regulation by microRNAs
- Regulation by riboswitches
- Regulation by translation factors
- Metabolic regulation (alosterism, feedback, regulation of pathways using bioengineering).

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Tod ThielLv2

27 Dec 2018

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2. Which increases fitness: a fitness tradeoff or an adaptation?

6. Which of these would be most likely to have a lot of cell junctions, which increase the structure of a tissue and enable communication? a. Connective tissue b. Epithelial tissue

10. Name some of the special cells or special modifications of epithelial cells.

11. Using an example for illustration, explain the mechanism in feedback regulation

beigereindeer647

Phosphofructokinase (PFK1) is a glycolytic enzyme that catalyzes the irreversible transfer of a phosphate from ATP to fructose -6-phosphate to form fructose-1, 6- bisphosphate.

fructose-6-phosphate + ATP --> fructose-1,6-bisphosphate + ADP

PFK1 is the key regulatory enzyme for glycolysis. When ATP levels are high in the cell, the cell no longer needs metabolic energy production to occur. In the case of these high energy levels, PFK1's activity is inhibited by allosteric regulation by ATP, which essentially closes the valve on the flow of carbohydrates through glycolysis.

Recall that allosteric regulators bind to a different site on the enzyme rather than the active (catalytic) site. ATP binds to the regulatory site and decreases PFK1 activity. ATP bound in the regulatory site acts as a modulator by lowering the affinity of PFK1 for its substrate, fructose-6-phosphate. AMP on the other hand, which is generated when the cell is in a low energy state binds to allosteric site and increases enzyme activity.

7. The enzyme PFK1 is an example of a non-regulatory enzyme or regulatory enzyme?

8. How is PFK regulated?

A. It is not regulated because it is a non-regulatory enzyme

B. allosteric enzyme regulation

C. covalent enzyme regulation

D. or proteolytic cleavage enzyme regulation?

9. What is the substrate and to which site on the enzyme does it bind? Which compounds are the positive and negative effectors?

10. In which conformational state would the enzyme be when negative inhibitors bind and in which conformational state would the enzyme be when positive inhibitors bind?

11. PFK1 is a heterotropic or homotropic regulatory enzyme?

12. Draw (or insert the picture from your course packet available on Canvas) the graph that corresponds to this reaction. Your graph should include the activity of PFK without bound effectors, with bound positive effector, and with bound negative effector. Label (or describe) each line to distinguish these along with which molecules are positive and negative effectors.

13. How does Vmax and K0.5 change with the positive and negative effectors?

1. Formation of Chromatin Loops in the nucleus might resultin

A. Transcriptional activation

B. Transcriptional repression

C. Epigenetic Regulation

D. Long range genomic interactions

E. All of the above

2. Which of the following statements is false?

A. All the muscle cells in human body express MyoD

B. All the cells in human body express MyoD and a few homeoticgenes

C. MyoD protein can transform few differentiated cells intomuscle cells

D. Pattern formation is controlled by specific genes

E. Morphogens are molecules that affect cell fate by theirdifferential expression

8. Which of the following questions could NOT be answered by theprocess of RNA

interference (RNAi)?

A. What is the function of gene OSU in a particular species of aspider?

B. What will happen in a particular insect's digestion if geneOHO is not able to be translated?

C. Is gene MICH expressed in individuals for a disorder inhumans?

D. Will the disabling of gene NEIL in Drosophila and ina mouse cause similar results?

E. None of the above

Please explain your answers.

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