Abstract
Endosomes are essential cellular stations where endocytic and secretory trafficking routes converge. Proteins transiting at endosomes can be degraded via lysosome, or recycled to the plasma membrane, trans-Golgi network (TGN), or other cellular destinations. Pathways regulating endosomal recycling are tightly regulated in order to preserve organelle identity, to maintain lipid homeostasis, and to support other essential cellular functions. Recent studies have revealed that both pathogenic bacteria and viruses subvert host endosomal recycling pathways for their survival and replication. Several host factors that are frequently targeted by pathogens are being identified, including retromer, TBC1D5, SNX-BARs, and the WASH complex. In this review, we will focus on the recent advances in understanding how intracellular bacteria, human papillomavirus (HPV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) hijack host endosomal recycling pathways. This exciting work not only reveals distinct mechanisms employed by pathogens to manipulate host signaling pathways, but also deepens our understanding of the molecular intricacies regulating endosomal receptor trafficking.
Highlights
Endocytosis is a key cellular step that mediates chemical information exchange between a cell and its extracellular environment
Many new factors have been identified, and novel functions have been uncovered for some classic endocytic recycling proteins
It is increasingly clear that the molecular machines that facilitate and regulate endocytic recycling represent targets for pathogenic factors produced by both intracellular bacteria and viruses
Summary
Endocytosis is a key cellular step that mediates chemical information exchange between a cell and its extracellular environment. Recent studies have uncovered that many intracellular bacteria, including Chlamydia trachomatis (Mirrashidi et al, 2015), Legionella pneumophila (Finsel et al, 2013), Salmonella Typhimurium (D’Costa et al, 2019), Burkholderia cenocepacia (Walpole et al, 2020), and Coxiella burnetii (Martinez et al, 2020), target host endosomal recycling pathways for their survival and replication (Table 1) These bacteria pathogens utilize different types of secretion systems and a plethora of effector proteins to create a unique vacuolar compartment known as pathogen vacuoles or inclusion, in which they can replicate. Delays phagosome maturation via F-actin Inhibits retromer activity Helps to position of Salmonella-containing vacuoles Unknown Promotes replication of C. burnetii
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