Introduction
The endoplasmic reticulum performs many disparate roles in the eukaryotic cell. The ER surrounds the nucleus forming the nuclear envelope. The ER extends out from the nuclear envelope into the cytoplasm in a continuous, membrane bound network. This network consists of two distinct domains; smooth tubular ER which form a spider web like network in the cell periphery, and rough (ribosome studded) flat sheet ER which generally occupy the center of the cell. The distinct morphology of these domains are thought to represent a division of labor. The smooth tubular ER is responsible for Ca2+ signaling, lipid synthesis, and membrane contact site formation\cite{Phillips2016}. The relatively ribosome rich sheet ER is responsible for the majority of the membrane bound and secreted protein synthesis as well as their folding and insertion into membranes.
The ER membrane provides an ideal scaffold in which the proteins ultimately responsible for all of these essential functions can operate efficiently\cite{Phillips2016,Voeltz2006}. The demands the cell places on the ER are spatiotemporally dynamic requiring that the scaffold membrane be equally dynamic\cite{Federovitch2005}. In times of increased demand or stress the ER membrane is able to expand, increasing its available surface area to provide more scaffolding space\cite{Yorimitsu2006,Cebollero2012}. For example, if a cell is stimulated to begin secreting a protein in large quantities the sheet ER would expand to accommodate more ribosomes and increase the production of the secreted protein\cite{Cebollero2012}. Equally important to these dynamics and ER function is the ER’s ability to reduce membrane after the need for increased production has passed. While ER expansions is relatively well understood comparatively little work has been done to understand ER shrinkage.
Autophagy is a process by which the cell is able to recycle organelles and other cellular components by degradation in the vacuole/lysosome. This occurs either by internalizing cargos into a double membraned autophagosome which eventually fuse with the vacuole/lysosome or through direct fusion of cargo with the vacuole/lysosome\cite{Glick2010}. Selective autophagy is distinct from the nonspecific autophagy that occurs during starvation where the cell recycles cellular components indiscriminately. It is a process where specific cellular components are marked for recycling either because they are obsolete or nonfunctional\cite{Zaffagnini2016}. ER autophagy or ERphagy, has been proposed as the method through which the ER is able to rid itself of unneeded and damaged membrane and protein aggregates. While selective autophagy of other organelles such as the mitochondrion are thoroughly studied ERphagy remains a poorly characterized process\cite{Ding2012}. In this review we will detail the limited advances that have been made in demonstrating the existence of ERphagy and understanding the signaling involved in its regulation. We will discuss the important implications of this work and some of the many questions that remain unanswered.