Cholera is an infectious disease that spreads in countries without clean drinking water or adequate sewage disposal. The bacterium causing the disease was identified in 1884. How it causes disease was discovered almost 100 years later.
A toxin produced by the bacterium changes the G-proteins in cells lining the intestine. The G-proteins become "stuck" in the activated—or turned on—state. They can't turn themselves off as they do when normally regulated. The effect is that water is pumped continuously out of the cells into the intestines, causing dangerously severe diarrhea.
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What Causes Cholera Normally, both the receptor and the amplifier span the membrane. The G-protein sits on the inner surface of the membrane. This current view is a little different from Rodbell's original model. In a person with cholera, the G-protein is stuck in the "on" position-next to the AC molecule
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Image: Courtesy of NIDDK
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Scientists have found a G-protein defect in one type of inherited night blindness. Persons with this condition have a mutation in the gene that codes for the G-protein found in the eye's rod cells. Scientists believe that this defective G-protein is overactive. It stays turned on more than it normally would, and the person can't see well at low light levels.
During the day, a similar system in the cone cells of the eyes allows us to see color. This system depends on a different G-protein. Thus, persons with night blindness have normal daytime vision.
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Light enters the eye (1) and strikes the rod cells in the retina (2). Light receptors, G-proteins and amplifiers are on discs within the rods (3)
When light strikes a light receptor, it activates a G-protein, which binds to an amplifier molecule. This sends a signal to the brain, resulting in light perception. G-proteins normally turn themselves off in a natural regulatory cycle. But in inherited night blindness, the G-protein stays on, interfering with normal vision.