What molecular features create the sensation of sweetness?

The sweetness receptor
Despite the wide variety of chemical substances known to be sweet, and knowledge that the ability to perceive sweet taste must reside in taste buds on the tongue, the biomolecular mechanism of sweet taste was sufficiently elusive that as recently as the 1990s, there was some doubt whether any single "sweetness receptor" actually exists.

The breakthrough for the present understanding of sweetness occurred in 2001, when experiments with laboratory mice showed that mice possessing different versions of the gene T1R3 prefer sweet foods to different extents. Subsequent research has shown that the T1R3 protein forms a complex with a related protein, called T1R2, to form a G-protein coupled receptor that is the sweetness receptor in mammals.

Sweet receptor pathway
To depolarize the cell, and ultimately generate a response, the body uses a different taste receptor pathway for each taste—sweet, sour, salty, bitter, umami, etc. Incoming sweet molecules bind to their receptors, which causes a conformational change in the molecule. This change activates the G-protein, gustducin, which in turn activates adenylate cyclase. Adenylate cyclase catalyzes the conversion of ATP to cAMP. The cAMP molecule then activates a protein kinase, which in turn phosphorylates and closes a potassium ion channel. The excess potassium ions increase the positive charge within the cell causing voltage-gated calcium ion channels to open, further depolarizing the cell. The increase in calcium ultimately causes neurotransmitter release, which is then received by a primary afferent neuron.