The phosphoinositide (PI) content of an internal membrane is a key regulator of intracellular trafficking. PIs recruit effector proteins to the membrane surface to coordinate signaling and trafficking inside the cell, this is particularly critical in the endosomal/lysosomal pathway where endosomes are sorted for recycling or degradation.The work presented here translates a mouse model of CMT4B2, Mtmt13-/-, into a robust in vitro system where lentivirus mediated expression of exogenous proteins can be used to better understand the roots of CMT4B2 myelin pathology.
