Although most lipid synthesis occurs in the ER, some lipid-modifying enzymes reside in other compartments.
As a result, the amount of lipid exchange between the ER and other organelles at MCSs could significantly affect lipid
homeostasis by regulating the rate at which a lipid substrate synthesized in the ER reaches an enzyme in another compartment.
An example is provided in studies on ER–plasma membrane contacts and their role in restoring phosphoinositide (PIP) levels in the plasma membrane following calcium signaling.
Phosphatidylinositol (PI) is synthesized in the ER and can be converted to PIPs in the plasma membrane.
It has been found that calcium signaling induces contacts between the ER and plasma membrane, which may promote PI transfer to the plasma membrane at these MCSs.
Once the PI reaches the plasma membrane, it can be converted to PIPs.
Thus, the formation of ER–plasma membrane contacts and the transfer of PI at these sites may regulate the rate of PIP formation in the plasma membrane.