Question

H₁

R₁
G-PAP
G
PP
TAP
Cell
Division
過一圈
R₂
G-PIP
H= Hormone
R= Membrane receptor
G = G protein
G-PAP= G-protein activating protein
G-PIP G-protein inactivating protein
=
PP= Phosphorylating protein
TAP Transcription activation protein
=
8. The diagram above represents a model of signal transduction pathways (I and II) in a cell that is targeted
by two different hormones (H, and H₂). The components of the signal transduction pathways are
identified in the figure legend. Each cellular molecule in both pathways can exist in an inactive or active
form. When the components in pathway I are sequentially activated, the TAP molecules promote cell
division. When the components in pathway II are sequentially activated, downstream signaling by the G
protein is inhibited. Based on the model, which of the following mutations is most likely to result in
a cell that will generate a cancerous tumor?
(A) A mutation in the gene encoding PP that results in a nonfunctional protein
(B) A mutation in the gene encoding G-PIP that results in a nonfunctional protein
(C) A mutation in the gene encoding R, so that it is inactive even in the presence of H₁
(D) A mutation in the gene encoding R₂ so that it is active even in the absence of H₂

Answer 1

A mutation in the gene encoding R₂ so that it is active even in the absence of H₂ is most likely to result in a cell that will generate a cancerous tumor. Option (D)

What does this scenario entail?

It describes a scenario where the receptor R₂ is constitutively active, meaning it's always turned on even without the presence of its ligand, H₂. This constitutive activation of R₂ would continuously activate the downstream signaling pathway, leading to the inhibition of G protein activity. This inhibition would prevent the normal activation of TAP molecules, which are responsible for promoting cell division.

In contrast, the other options describe mutations that would disrupt or disable components of either signal transduction pathway. While these mutations could have various cellular effects, they would not directly lead to the constitutive activation of R₂ and the consequent inhibition of cell division control.

Therefore, a mutation in the gene encoding R₂ so that it is active even in the absence of H₂ is the most likely mutation to trigger uncontrolled cell division and potentially lead to cancer development.