Mutations in which protein are associated with bradyopsia?

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Multiple Choice

Mutations in which protein are associated with bradyopsia?

Explanation:
Bradyopsia reflects a problem with turning off the photoreceptor signal quickly after light hits. In the rod cell, once rhodopsin is activated it triggers transducin to activate PDE6, lowering cGMP and closing channels, which hyperpolarizes the cell. To reset, transducin must be turned off fast, a job done by a transducin-inactivating protein that speeds up GTP hydrolysis on transducin. If mutations disrupt this inactivating protein, transducin stays active longer, PDE6 keeps signaling, and the cells take longer to return to their baseline state. The result is a delayed recovery of vision after light exposure, which is what bradyopsia is. Other proteins like rhodopsin or PDE6 affect different parts of the cascade (activation or overall signaling), but bradyopsia specifically stems from defective shutoff due to mutations in the transducin-inactivating protein.

Bradyopsia reflects a problem with turning off the photoreceptor signal quickly after light hits. In the rod cell, once rhodopsin is activated it triggers transducin to activate PDE6, lowering cGMP and closing channels, which hyperpolarizes the cell. To reset, transducin must be turned off fast, a job done by a transducin-inactivating protein that speeds up GTP hydrolysis on transducin. If mutations disrupt this inactivating protein, transducin stays active longer, PDE6 keeps signaling, and the cells take longer to return to their baseline state. The result is a delayed recovery of vision after light exposure, which is what bradyopsia is. Other proteins like rhodopsin or PDE6 affect different parts of the cascade (activation or overall signaling), but bradyopsia specifically stems from defective shutoff due to mutations in the transducin-inactivating protein.

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