Question

1) Epinephrine (adrenaline) stimulates glycogen breakdown in skeletal muscle cells and can also inhibit transcription of a gene that causes glycogen synthesis. What types of signaling does epinephrine mediate and how does the G-protein get activated?

2) Compare the speed of these two cellular responses and why they are different.

3) Outline the signaling pathway in both cases and explain how one hormone using the same G-protein coupled receptor can causes these two different cellular response in the same cell. Hint: think about the secondary messenger produced.

4) Epinephrine also causes an increase in heart-rate and contraction in the heart. What explains how this same hormone can have such a different cellular response in a different tissue? Hint: think about the secondary messengers produced.

5) Describe 2 different ways that a gain of function in a receptor tyrosine kinase receptor could lead to increased growth and/or survival for a cancer cell.

Answer 1

Answer:

(1) Several hormones greatly affect glycogen metabolism. Glucagon and epinephrine trigger the breakdown of glycogen. Muscular activity or its anticipation leads to the release of epinephrine (adrenaline), a catecholamine derived from tyrosine, from the adrenal medulla. Epinephrine markedly stimulates glycogen breakdown in muscle and, to a lesser extent, in the liver. The liver is more responsive to glucagon, a polypeptide hormone that is secreted by the α cells of the pancreas when the blood-sugar level is low. Physiologically, glucagon signifies the starved state.

The signal molecules epinephrine and glucagon bind to specific 7TM receptors in the plasma membranes of muscle and liver cells, respectively. Epinephrine binds to the β-adrenergic receptor in muscle, whereas glucagon binds to the glucagon receptor. These binding events activate the α subunit of the heteromeric Gs protein. A specific external signal has been transmitted into the cell through structural changes, first in the receptor and then in the G protein.

The GTP-bound form of the α subunit of Gs activates adenylate cyclase, a transmembrane protein that catalyzes the formation of the secondary messenger cyclic AMP from ATP.