get help please with this question?  Two mutations have occurred to proteins within the glucagon signaling pathway: A) The glucagon receptor has a mutation. This mutation causes this GPCR to always have a conformation that will induce nucleotide exchange for any associated heterotrimeric G proteins, even without glucagon binding to the receptor.  B) The alpha subunit of the heterotrimeric G protein has a mutation. This mutation causes the Gαarginine finger to always be in a position to properly order the catalytic residues within the Gαsubunit to promote catalysis. Question: What will the combined effect of both mutations be on the signaling pathway and what is the mechanistic reason for this effect

Human Anatomy & Physiology (11th Edition)
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Can I get help please with this question? 

Two mutations have occurred to proteins within the glucagon signaling pathway:

A) The glucagon receptor has a mutation. This mutation causes this GPCR to always have a conformation that will induce nucleotide exchange for any associated heterotrimeric G proteins, even without glucagon binding to the receptor. 

B) The alpha subunit of the heterotrimeric G protein has a mutation. This mutation causes the Gαarginine finger to always be in a position to properly order the catalytic residues within the Gαsubunit to promote catalysis.

Question: What will the combined effect of both mutations be on the signaling pathway and what is the mechanistic reason for this effect?

Expert Solution
Step 1

Upon activation by a ligand, the GPCR undergoes a conformational change and then activate the G proteins by promoting the exchange of GDP/GTP associated with the Gα subunit.

This leads to the dissociation of Gβ/Gγ dimer from Gα. Both these moieties then become free to act upon their downstream effectors.

The GPCR is turned on due to mutation and thus dissociation of Gβ/Gγ dimer from Gα is unstoppable.

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