G Protein Coupled Receptors

Mutations within genes coding for G protein-coupled receptors (GPCRs) can lead to one of two major outcomes—a loss-of-function or a gain-of-function. Loss-of-function mutations prevent signaling in GPCR pathways, even in the presence of signaling molecules. Gain-of-function mutations activate signaling in GPCR pathways, even in the absence of signaling molecules.

Which of the following will most likely be found in an individual with a gain-of-function GPCR mutation?

• Signal transduction pathways that are activated even if ligand-to-receptor binding does not occur

• Signal transduction pathways that are inactive if ligand-to-receptor binding does not occur

• Signal transduction pathways that are activated only if ligand-to-receptor binding occurs

• Signal transduction pathways that are inactive even if ligand-to-receptor binding occurs

The information below shows and describes the intermediate steps of the MAPK/ERK signaling cascade. After MEK is activated, it phosphorylates and activates ERK. ERK goes on to phosphorylate and activate a variety of target molecules, including transcription factors like c-Myc that promote cell growth and division.

Which of the following toxins will most likely inhibit the phosphorylation of c-Myc?

• A toxin that prevents the phosphorylation of ERK

• A toxin that prevents the dephosphorylation activity of MEK

• A toxin that prevents the removal of a phosphate group from ERK

• A toxin that prevents c-Myc from activating ERK

The bacterium Vibrio cholerae causes cholera, an infectious disease that often leads to severe dehydration as a result of ongoing diarrhea. During an infection, Vibrio cholerae releases a protein complex called cholera toxin.

After its release, cholera toxin enters intestinal epithelial cells and binds to a G protein. This causes the G protein to be permanently activated. The downstream effects of this G protein activation are shown in the signal transduction pathway below.

Based on the information above, which of the following correctly describes cholera toxin and its effect on intestinal epithelial cells?

• Cholera toxin is an extracellular signal that decreases adenylyl cyclase activity.

• Cholera toxin is an intracellular signal that increases extracellular chloride ion concentration.

• Cholera toxin is an intracellular signal that decreases intracellular cAMP concentration.

• Cholera toxin is an extracellular signal that increases the dephosphorylation of protein kinase A.

Each mammalian olfactory neuron appears to use the same machinery for transducing signals from its odorant receptor molecules. Upon odorant binding, the receptor is thought to activate G_olf, a G protein. G_olf-mediated activation of adenylate cyclase III then raises intracellular cAMP levels, causing a cyclic-nucleotide-gated channel to open. The influx of cations through this channel ultimately leads to the formation of an action potential, which allows the primary neuron to signal to the brain.

Which of the following scientific questions would best help researchers determine how the mutation prevents the activation of G_olf?

• Does the mutation prevent the entry of cations through the cyclic-nucleotide-gated channel?

• Does the mutation prevent ligand binding on the odorant receptor?

• Does the mutation prevent the conversion of ATP to cAMP?

• Does the mutation prevent the activity of adenylate cyclase III?

Which of the following is true regarding these cell receptors?

• Ligand-gated ion receptors are receptors for a group of signaling molecules called growth factors.

• Binding of a ligand to receptor tyrosine kinases causes a direct change in ion distribution across a membrane.

• G protein-coupled receptors (GPCRs) are the most diverse type of cell receptor.

• Intracellular receptors can be found in the cytoplasm or nucleus.

A cell releases chemical signals into its surrounding space in order to communicate with neighboring cells.

Which of the following must occur for the communication to be successful?

• The neighboring cell must have the right receptor to receive the signal.

• The chemical signal must bind to hormones on the neighboring cells.

• The neighboring cells must be able to absorb the chemicals through diffusion.

• The same chemical signal must be produced within the neighboring cells.