The invasion of tobacco mosaic virus RNA induces endoplasmic reticulum stress-related autophagy in HeLa cells

Li, Li; Wang, Li; Xiao, Ruijing; Zhu, Guoguo; Li, Yan; Liu, Changxuan; Yang, Ru; Tang, Zhiqing; Li, Jie; Huang, Wei; Chen, Lang; Zheng, Xiaoling; He, Yuling; Tan, Jinquan

Based on the EM studies, we concluded that the membranes of autophagic vacuoles originated from expanded ER membranes. Recently, some EM studies have also shown that autophagosomal membranes originate from the ER or are contiguous with it. For example, Bernale et al. [33] discovered that ER proliferation was accompanied by the formation of autophagosomal-like structures that were densely and selectively packed with membrane stacks derived from the UPR (unfolded protein response)-expanded ER. Ueno et al. [43] showed that ER membrane markers were pre-served in autophagic vacuolar membranes isolated from the rat liver vacuoles of animals administered leupeptin. Axe et al. [44] reported that autophagosomal formation from membrane compartments enriched in phosphatidylinositol 3-phosphate was dynamically linked to the ER and that a ring-like particle (termed an omegasome) formed, indicating that the autophagosome formed in close association with the ER. Herein, we also described a likely process of TMV-RNA-induced autophagy ( Figure 6B) . A series of electron micrographs provided potent evidence for the expansion of ER membranes into mature autophagosomes. Thus we conclude that ERS stimulates ER membranes to expand and form autophagosomes.