Mutation in PLC that allows it to bind to Yes the Gos subunit, but prevents it f

Question

Mutation in PLC that allows it to bind to Yes the Gos subunit, but prevents it from releasing the Gos subunit afterwards Phospholipase C, PLC, is an effector protein that is able to form 2 secondary messengers, lP3 and DAG through the hydrolysis of phosphoester bond in certain phospholipids The IP3 stays in the cytoplasm while the diacylglycerol, DAG, is in the plasma membrane. The function of DAG and IPS is to elevate the calcium levels in the cytoplasm and the mitochondrial matrix. By increasing the levels of calcium, PKC can be activated If there is a mutation in PLC that allows it to bind to the Gos subunit, but prevents it from releasing the Gos subunit afterwards, glycogen breakdown is going to be affected When the Gas subunit binds to the PLC, the PLC is activated. As a result, the secondary messengers, lP3 and DAG are created. IP3 opens IP3-gated Ca channels in the ER membrane resulting in the release of stored Ca2 ions into the cytosol. The rise in cytosolic Ca recruits PKC to the plasma membrane RKC istbenwactivated by DAG. Activated PKC can help stimulate glycogen breakdown. However, since the PLC cannot release the Gas subunit after it creates IP3 and DAG, the Gwas subunit is unable to be "recycled." In other words, the Gos subunit has GIPase, activity where it is able to bind to GTP and GDP. When the Gas subunit is bound to GDP, the Gas subunit can bind to the GYB subunit. This trimeric, Gs protein can bind to an active receptor. Yet, since the PLC is preventing the Gos subunit from being reused, minimal glycogen breakdown is going to OCCur

Explanation / Answer

yes the answer is right as it talks about DAG and IPG increasing the calcium levels which happens of glycogen breakdown which has been mentioned in the answer.SO it is a complete answer and PLC does not release Gas.

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