When adrenaline binds to adrenergic receptors on the surface of a muscle cell, it activates a G-protein, initiating a signaling pathway where the activated G α subunit activates adenylyl cyclase, increasing cAMP levels in the cell; the cAMP molecules then activate a cAMP-dependent kinase 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 G-protein signaling pathway. Indicate how glycogen levels would be affected in the presence of adrenaline in the following cells. Would they be higher, lower, or the same as normal cells that are treated with adrenaline?
o In cells that have a G α subunit that cannot hydrolyze GTP but can interact properly with G β and G γ.
• In cells that lack the receptor?
• In cells that lack adenylyl cyclase?
• In cells that lack cAMP phosphodiesterase?