A fundamental question of cell signaling biology is how faint external signals produce robust physiological responses. One universal mechanism relies on signal amplification via intracellular cascades mediated by heterotrimeric G-proteins. This high amplification system allows retinal rod photoreceptors to detect single photons of light. Although much is now known about the role of theα-subunit of the rod-specific G-protein transducin in phototransduction, the physiological function of the auxiliary αβ-complex in this process remains a mystery. Here, we show that elimination of the transducin γ-subunit drastically reduces signal amplification in intact mouse rods. The consequence is a striking decline in rod visual sensitivity and severe impairment of nocturnal vision. Our findings demonstrate that transducin αβ-complex controls ignal amplification of the rod phototransduction cascade and is critical for the ability of rod photoreceptors to function in low light conditions.