Question

You are interested in cell-size regulation and discover that signaling through a GPCR called ERC1 is important in controlling cell size in embryonic rat cells. The G protein downstream of ERC1 activates adenylyl cyclase, which ultimately leads to the activation of PKA. You discover that cells that lack ERC1 are 15?

1) addition of a drug that causes cyclic AMP phosphodiesterase to be hyperactive
2) addition of a drug that prevents GTP hydrolysis by Gα
3) addition of a drug that activates adenylyl cyclase
4) addition of a drug that mimics the ligand of ERC1

Answer 1

The most effective method to increase cell size in the absence of the ERC1 receptor is to add a drug that mimics the ERC1 ligand, directly engaging the specific pathway for cell regulation.

Step-by-step explanation:

Signal transduction pathways regulate cell size by transmitting external signals into cell responses. In the scenario described, the GPCR ERC1's downstream signaling involves the activation of adenylyl cyclase, which then leads to the production of cAMP, subsequently activating Protein Kinase A (PKA). In cells lacking ERC1, the pathway starting from ERC1 to PKA would be disrupted, leading to smaller cell sizes.

Option 1, the use of a drug causing hyperactive cyclic AMP phosphodiesterase, would further reduce cAMP levels, aggravating the problem. Option 2, preventing GTP hydrolysis by Gα, would lead to prolonged activation of the G protein, which is not specific to the intended pathway. Option 3, activating adenylyl cyclase, could be beneficial but it is not as direct as option 4. The addition of a drug that mimics the ERC1 ligand would engage the specific pathway intended for cell size regulation, thereby compensating for the lack of the native ERC1 signal and restoring function closer to physiological norms.