When brassinosteroids bind a receptor on the cell's surface, an intracellular enzyme called BIN2 is inactivated by an unknown mechanism. Previously, investigators thought that inactivation of BIN2, which is a kinase, freed a second protein known as BES1 from entrapment in the cytoplasm, the watery compartment surrounding a cell's nucleus, and allowed it to migrate or "shuttle" into the nucleus where it tweaked the activity of genes regulating plant growth.
A closer inspection, however, revealed that BIN2 resides in multiple compartments of a cell, including the nucleus, and it is there--not in the cytoplasm--that BIN2 meets up with BES1 and prevents it from activating growth genes. "All of a sudden the 'BES1 shuttle model' no longer made sense," says Vert, adding that it took many carefully designed experiments to convince himself and others that it was time to retire the old model.
A new picture of how brassinosteroids stimulate plant growth now emerges based on those experiments: steroid hormones are still thought to inactivate BIN2 and reciprocally activate BES1, but instead of freeing BES1 to shuttle into the nucleus, it is now clear that the crucial activation step occurs in the nucleus where BES1 is already poised for action. Once released from BIN2 inhibition, BES1 associates with itself and other regulatory factors, and this modified form of BES1 binds to DNA, activating scores of ta