Cellular stressors typically induce two protective counter-responses-autophagy and the unfolded protein response (UPR). It is conceivable that these two endoplasmic reticulum (ER) membrane-based processes would intersect/interact somehow with the constitutive housekeeping process of exocytic membrane traffic from the ER. How exactly might this occur? Recent evidence indicates that a conserved Rab protein, Rab1/Ypt1p, has functional roles in UPR and autophagy. This molecular switch and its associated effectors may therefore serve to link up a network of cellular responses to stress through changes in membrane dynamics and protein turnover. The notion provides further explanations as to why elevation of Rab1/Ypt1p levels could counter the cytotoxicity of α-synuclein, and a similar mode of protection may well be at work against other stresses.
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