Cell Signaling

Question 1

Name the two key components required for cell-cell communication.

Answer 1

A signaling molecule and a receptor

Question 2

Explain how a cell can respond in a specific way to an environment that contains a
multitude of different signaling molecules.

Answer 2

If an environment has a multitude of signaling molecules for which the cell bears receptors, the cell will respond to all of them, resulting in an overall change in behavior.

Question 3

Explain how a single signaling molecule can have different effects on different target
cells.

Answer 3

Different target cells can have different receptors, and even if they don’t, the cells may have been programmed to respond differently to that specific signal-receptor binding interacting.

Question 4

Two cells are right next to each other. One has a membrane-bound signaling molecule, and the other bears that signal’s receptor.

This type of signaling is called:

a) synaptic
b) contact-dependent
c) endocrine
d) paracrine

Answer 4

b) contact-dependent

Question 5

A signaling cell releases a local mediator, which then binds to multiple target cells.

This type of signaling is called:

a) synaptic
b) contact-dependent
c) endocrine
d) paracrine

Answer 5

d) paracrine

Question 6

A neuron releases a neurotransmitter onto target cells.
This type of signaling is called:

a) synaptic
b) contact-dependent
c) endocrine
d) paracrine

Answer 6

a) synaptic

Question 7

A hormone-producing cell releases a hormone into the bloodstream. The hormone then binds to a target cell.

This type of signaling is called:

a) synaptic
b) contact-dependent
c) endocrine
d) paracrine

Answer 7

c) endocrine

Question 8

Describe autocrine signaling

Answer 8

A molecule is released from a cell and then binds to receptors on that same cell, or to nearby cells of the same type.

Question 9

Describe the cellular signaling mechanisms
that occur when a signaling molecule binds
to a receptor that activates the Gi protein

Answer 9

When activated, Gi-alpha inhibits adenylyl cyclase. Gi-beta-gamma can also activate certain potassium channels.

Question 10

What types of hormones have intracellular receptors.

Answer 10

Small, hydrophobic molecules that can diffuse through the membrane

Question 11

What is the difference between “early primary” and “delayed secondary” responses induced by activation of a nuclear hormone receptor.

Answer 11

Primary/early response refers to the increased transcription of primary response genes. This occurs after the signal-receptor dimers have bound DNA.

In secondary/delayed response, some of the primary response proteins translated earlier are transcription factors. They in turn stimulate transcription of of other genes.

Question 12

Describe the general structural features of the nuclear receptor superfamily.

Answer 12

They have a ligand binding domain near the C terminus, a DNA-binding domain, and the transcription-activating domain at the amino terminus.

Question 13

Explain two different types of signal transduction associated with enzyme coupled receptors

Answer 13

1.) Dimerized signal binds two receptors, catalytic domain activated.
OR
2.) Signal binds one subunits of a receptor, and another subunit as well as an associated enzyme becomes activated.

Question 14

Indicate how the term “signal transducer” adequately

describes the function of cell-surface receptor proteins.

Answer 14

“Signal transducer” is an accurate term because despite the receptor itself not leaving the membrane, the cell undergoes changes in response.

Question 15

Explain the method of signal transduction associated with ion-coupled receptors.

Answer 15

Ion-coupled - a signal binds the receptor, conf. change, ions can now flow into cell.

Question 16

Describe the general structural features of a G-protein.

Answer 16

Trimeric, has an alpha, beta and gamma subunits. Alpha and gamma subunits are tethered to the membrane.
Alpha bound to GDP = inactive
Alpha bound to GTP = active

Question 17

Describe the general structural features of a G-

protein-linked cell surface receptor.

Answer 17

Seven transmembrane helices with an extracellular signal receptor site and an intracellular region that interacts with G-proteins.

Question 18

Describe how a receptor “activates” a G-protein.

Answer 18

When a signal binds a GPCR, the receptor induces a conf. change on the G-protein, releasing GDP. The alpha subunit then binds GTP.
Now activated, the G-protein dissociates from the GPCR, and the alpha receptor and/or the beta-gamma dimer can then activate specific enzymes or ion channels.

Question 19

Describe how, after a period time, the G-protein inactivates itself.

Answer 19

Eventually, the GTP on the alpha-subunit is hydrolyzed, and the G-protein is inactivated.

This inactivation can be accelerated by the protein’s targets or by RGS proteins.

Question 20

Describe the structure of cyclic AMP, how it is synthesized, and how it is degraded.

Answer 20

cAMP= adenine bound to deoxyribose, in turn bound to three of the oxygens on phosphate
5’ AMP is linear.

cAMP is synthesized from ATP and can be hydrolyzed to 5’ AMP by cAMP phosphodiesterase.

Question 21

Describe how adenylyl cyclase is activated via a Gs-coupled receptor. (Gs= stimulatory G-protein)

Answer 21

When a signaling molecule binds to a GPCR that is

coupled to Gs, the activated alpha subunit translocates to adenylyl cyclase to activate it.

Question 22

How does cyclic AMP activate protein kinase A.

Answer 22

PKA consists of a regulatory subunit and a catalytic subunit. When cAMP binds the regulatory subunit, the catalytic subunits dissociate from it and are activated.

Question 23

Describe how PKA recognizes, and then alters the function of, specific proteins in the
cell.

Answer 23

PKA recognizes serine and threonine in select proteins and phosporylates them. This alters the function of said proteins. The protein is now more hydrophobic.

Question 24

Describe how cyclic AMP, acting through PKA, can alter gene transcription.

Answer 24

PKA can phosphorylate CREB in the nucleus. CREB can then bind to a CRE (response element)

Question 25

Discuss the role of the serine/threonine phosphoprotein phosphatases in signal
transduction.

Answer 25

Ser/Thr phosphatases reverse the actions of PKA by removing the phosphate groups.

Question 26

Describe a mechanism for desensitizing a G-protein coupled receptor.

Answer 26

Phosphorylation by GRK’s, attract an arrestin to bind and block g-proteins from associating with GPCR.

GPCR can also be endocytosed.

Question 27

Describe the mechanism by which cholera toxin causes a large increase in intestinal epithelial cell cyclic AMP levels.

Answer 27

The cholera toxin puts an ADP ribose group on the G-alpha subunit. In this case, this stops Gs from hydrolyzing GTP, thus keeping it in the active form. This results in a large increase of cAMP and PKA in intestinal epithelial cells. PKA then phosphorylates the CFTR chloride channel, thus activating it. Na absorbtion is also inhibited.
This results in lots of water rushing into the intestinal lumen = diarrhea.