Umami Phospholipase C GTP PLP Na* TIRI TIR3 ??? IPs Ca channel Endoplasmic retic
ID: 301014 • Letter: U
Question
Umami Phospholipase C GTP PLP Na* TIRI TIR3 ??? IPs Ca channel Endoplasmic reticulumm 1. You find a mutant strain of mouse that responds very weakly to the umami taste (receptor and pathway above). You isolate Umami receptors from the taste buds and perform a series of experiments (10 pts.) In the set of experiments, you find that the receptor is successfully binding umami molecules, and that Phospholipase C is successfully liberating PIP2 from the membrane to create IPs. Given this information what would you predict is causing the defective taste sense? (You can assume general proteins like the Na-K-ATPase pump work). Explain your reasoning by walking through the affected steps of the pathway.Explanation / Answer
According to the information, the umami taste sense gets activated via the phospholipase C-mediated PIP3 activation and downstream signalling cascade in the cells. The final effector molecule of this cyclic set of events must lead to activation of the calcium channel gates at the endoplasmic reticulum which release cytoplasmic calcium ions. These calcium ions then bring about channelization of the sodium-potassium pump by regulating a potential difference across the plasma membrane.
Considering that the sodium-potassium pump is functioning fine, the possible reason behind the failure of sense of taste in these mice could be a defective calcium channel gating system in the endoplasmic reticulum. In fact, studies have shown that the failure of optimized release of calcium from the endoplasmic reticulum not only brings about pathologies in the cell but also devastates the underlying secondary signalling mechanisms. Failure to sense the taste of umami remains one of them.
Hence, the defective endoplasmic reticulum mediated calcium channeling might be the possible reason behind this pathology.
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