The following excerpt and image come from a scientific paper written by Ebrahimi & Chess. They discuss the role of G proteins in olfaction, or the sense of smell.
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 Golf_\text{olf}​start subscript, start text, o, l, f, end text, end subscript, a G protein. Golf m_\text{olstart subscript, start text, o, l, f, end text, 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.
A mutation in a component of this signal transduction pathway prevents the cyclic-nucleotide-gated channel from opening.
Which of the following scientific questions would best help researchers understand how the mutation prevents the cyclic-nucleotide-gated channel from opening?
- Does mutation cause the influx of cations into the cell?
- Does mutation stimulate the conversion of ATP to cAMP?
- Does the mutation block the activation of adenylate cyclase III?
- Does mutation cause intracellular cAMP level to rise?
Does the mutation block the activation of adenylate cyclase III?