PHILADELPHIA (May 6, 2013) Researchers at the Monell Center and collaborators have identified a protein that is critical to the ability of mammals to smell. Mice engineered to be lacking the Ggamma13 protein in their olfactory receptors were functionally anosmic unable to smell. The findings may lend insight into the underlying causes of certain smell disorders in humans.
"Without Ggamma13, the mice cannot smell," said senior author Liquan Huang, PhD, a molecular biologist at Monell. "This raises the possibility that mutations in the Ggamma13 gene may contribute to certain forms of human anosmia and that gene sequencing may be able to predict some instances of smell loss."
Odor molecules entering the nose are sensed by a family of olfactory receptors. Inside the receptor cells, a complex cascade of molecular interactions converts information to ultimately generate an electrical signal. This signal, called an action potential, is what tells the brain that an odor has been detected.
To date, the identities of some of the intracellular molecules that convert odor information into an action potential remain a mystery. Suspecting that a protein called Ggamma13 might be involved, the research team engineered mice to be lacking this protein and then tested how the 'knockout' mice responded to odors.
Importantly, because the Ggamma13 protein plays critical roles in other parts of the body, the Ggamma13 'knockout' was confined exclusively to smell receptor cells. This specificity allowed the researchers to characterize the effect of Ggamma13 deletion on the olfactory system without interference from changes in other tissues.
Both behavioral and physiological experiments revealed that the Ggamma13 knockout mice did not respond to odors. The findings were published in the Journal of Neuroscience.
In behavioral tests, control mice with an intact sense of smell were able to detect and retrieve a piece of bu
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Monell Chemical Senses Center