Question

When adrenaline binds to adrenergic receptors on the surface of a muscle cell, it activates a G protein, initiating an intracellular signaling pathway in which the activated α subunit activates adenylyl cyclase, thereby increasing cAMP levels in the cell. The cAMP molecules then activate a cAMP-dependent kinase (PKA) that, in turn, activates enzymes that result in the breakdown of muscle glycogen, thus lowering glycogen levels. You obtain muscle cells that are defective in various components of the signaling pathway. Indicate how glycogen levels would be affected in the presence of adrenaline in the following cells. Would they be higher or lower than in normal cells treated with adrenaline? A. cells that lack adenylyl cyclase B. cells that lack the GPCR C. cells that lack cAMP phosphodiesterase

Answer 1

Glycogen levels would be higher in cells lacking adenylyl cyclase or the GPCR because these cells cannot activate PKA to break down glycogen. Conversely, glycogen levels would be lower in cells lacking cAMP phosphodiesterase, as prolonged PKA activation would increase glycogen breakdown.

Step-by-step explanation:

When adrenaline binds to adrenergic receptors on a muscle cell, it triggers a series of events leading to the breakdown of glycogen. This pathway involves a G protein activating adenylyl cyclase, which increases cyclic AMP (CAMP) levels, then CAMP activates protein kinase A (PKA), and PKA activates enzymes for glycogen breakdown. Now let's examine how cells with defective components would behave in the presence of adrenaline compared to normal cells.

• Cells that lack adenylyl cyclase: These cells would be unable to convert ATP to CAMP when the G protein is activated, leading to a failure to activate PKA. As a result, the downstream enzymes involved in glycogen breakdown would not be activated, and glycogen levels would be higher compared to normal cells treated with adrenaline.
• Cells that lack the GPCR: Without the G protein-coupled receptor, there would be no initiation of the signaling pathway in response to adrenaline binding. This would prevent adenylyl cyclase from being activated, no increase in CAMP, and no activation of PKA. Glycogen levels would therefore be higher in these cells compared to normal cells under the influence of adrenaline.
• Cells that lack cAMP phosphodiesterase: This enzyme is responsible for breaking down CAMP. In its absence, CAMP levels would remain elevated for a longer period, leading to prolonged PKA activation. Consequently, there would be enhanced glycogen breakdown, resulting in lower glycogen levels compared to normal cells upon adrenaline stimulation.