Figure 7: Normal mode analysis of the complex suggests a rack&pinion model for the signal transduction.

Retinal isomerization leads to breaking of the receptor into two domains that move in the opposite directions perpendicular to the membrane (1); shift of its transmembrane helices relative to each other creates a hydrophobic mismatch that has to be compensated through a tilt rotation of NpSRII (2) around the intracellular point of contact between NpSRII and NpHtrII (3); this motion levers TM1 and TM2 of the conjugated NpHtrII for a piston-like shift towards the cytosol (4), which concomitantly drags the helices of the other protomer, reversing the mechanism in the symmetric counterpart of the receptor (5) and (6). Solid black lines illustrate the approximate membrane boundaries with “IC” designating the intracellular side and “EC” designate the extracellular side.