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

Autophagy is a conserved pathway that functions in all eukaryotic organisms to maintain cellular homoeostasis. The autophagy pathway targets both cellular cytoplasmic constituents (such as damaged or surplus organelles, proteins and protein aggregates) for lysosomal degradation as well as microbial invaders (including viruses). Molecular steps are required for autophagosomal formation that involves a double-layered vesicle that fuses with a lysosome to digest the material inside the vacuole [17] . It is known that viral infection of a cell may stimulate autophagy [18] . Ubiquitin-like LC3 (light-chain protein 3) has been used as a specific marker for the autophagosomal compartment. Two forms of LC3, the cytosolic LC3-I and the membrane-bound LC3-II, are produced post-translationally. LC3-I is formed by the removal of the C-terminal 22 amino acids from newly synthesized LC3, followed by the conversion of a fraction of LC3-I into LC3-II. The induction of autophagy leads to the processing of LC3-I into LC3-II and its subsequent targeting to pre-autophagosomal and autophagosomal membranes [19] . Beclin1 is a mammalian autophagy gene, and its increased expression suggests increased cellular autophagic activity. In addition, Beclin1 can also bind to Bcl-2 and inhibit tumorigenesis, is monoallelically deleted in human breast and ovarian cancers and is expressed at reduced levels in the latter tumours [20, 21] .