wn to about 900 candidates," she said.
Huang then used a technique called reverse transcriptase polymerase chain reaction (RT-PCR) to find which of the candidates were expressed specifically in taste receptor cells. Of the approximately 30 proteins identified through RT-PCR, Huang searched for genes that were expressed in a small population of taste receptor cells -- the pattern that Zuker's and Ryba's team had previously discovered with taste receptors for sweet, bitter, and umami.
The researchers' attention was drawn immediately to a receptor molecule known as PKD2L1, which is related to a large family of proteins that shuttle ions into and out of cells. As predicted for a candidate sour receptor, PKD2L1 was not found in the cells that express the receptors for sweet, bitter, and umami, but instead was found in a novel population of taste cells. "Our fundamental premise was that salt and sour were going to be mediated by dedicated cells," said Zuker, "and those candidate receptors should not be present in sweet-, bitter-, or umami-sensing cells."
To link the receptors with the taste of sour, Zuker and his colleagues turned to another clever experimental strategy. Using a special mouse strain, they created genetically engineered mice that produced a diphtheria toxin in cells that expressed PKD2L1, thus killing the cells. They then recorded the nerve signals and tongue function coming from taste cells in the genetically-engineered mice. Remarkably, no matter what sour compounds they fed the mice, nerve signals from the taste cells remained absent; the animals were completely insensitive to all kinds of acids. But these "sourless" mice continued to be able to taste sweet, bitter, umami, and salt. "Killing these cells and showing that the mice now are totally unable to detect sour proved that these cells are the sensors for sour taste, and that indeed no other taste cells detect sour," said Zuker.
In an interesting extension of Page: 1 2 3 Related medicine news :1
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