Abstract

The endoplasmic reticulum (ER) is an essential organelle in cells that synthesizes, folds and modifies membrane and secretory proteins. It has a crucial role in cell survival and growth, thus requiring strict control of its quality and homeostasis. Autophagy of the ER fragments, termed ER-phagy or reticulophagy, is an essential mechanism responsible for ER quality control. It transports stress-damaged ER fragments as cargo into the lysosome for degradation to eliminate unfolded or misfolded protein aggregates and membrane lipids. ER-phagy can also function as a host defense mechanism when pathogens infect cells, and its deficiency facilitates viral infection. This review briefly describes the process and regulatory mechanisms of ER-phagy, and its function in host anti-microbial defense during infection.

Highlights

  • The endoplasmic reticulum (ER) is the largest membranous organelle in eukaryotic cells and consists of continuous lamellar and tubular structures spanning the cytoplasm

  • Mouse embryonic fibroblasts (MEFs) from Fam134b knockout mice infected with the Ebola virus showed a 10- to 100-fold increase in viral yield and an elevated expression of viral GP, VP40, and nucleocapsid proteins, indicating that Fam134bdependent ER-phagy restricts the virus replication (Chiramel et al, 2016)

  • Recent studies have shown that its knockdown enhances FAM134B-dependent ERphagy in cells infected with dengue virus (DENV) and Zika viruses (ZIKVs), increases ER degradation, reduces viral acquisition of ER membranes for replication, and prevents viruses survival

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Summary

Introduction

The endoplasmic reticulum (ER) is the largest membranous organelle in eukaryotic cells and consists of continuous lamellar and tubular structures spanning the cytoplasm. Recent studies have found that ER-phagy is involved in the process of microbial infections, but its functions, regulatory mechanisms, and interplay with pathogens still need further investigation (Reggio et al, 2020).

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