title: Atg4B(C74A) hampers autophagosome closure: a useful protein for inhibiting autophagy.
abstract: Recently we have reported that overexpression of an inactive mutant of Atg4B, a protease that processes pro-LC3 paralogues, inhibits lipidation of LC3 paralogues and autophagic degradation in mammalian cell. Through a mechanistic analysis, it was revealed that excess Atg4B mutant sequesters LC3 paralogues and blocks formation of Atg7-LC3 intermediate. Upon trap of LC3 paralogues, Atg5-positive autophagic structures accumulated. The structures are defective in the final closing step in autophagosome formation. The ability of the excess Atg4B mutant to inhibit autophagy provides not only an opportunity for further analysis of the LC3 system but also a useful tool available for a wide variety of experimental systems used in the study of autophagy.
authors.affiliation: Department of Cellular Regulation, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
authors.forename: Naonobu
authors.initials: N
authors.lastname: Fujita
authors.forename: Takeshi
authors.initials: T
authors.lastname: Noda
authors.forename: Tamotsu
authors.initials: T
authors.lastname: Yoshimori
mesh_terms: D000818:Animals; D001343:Autophagy; D003546:Cysteine Endopeptidases / Q000378:metabolism*; D006801:Humans; D008954:Models, Biological; D050505:Mutant Proteins / Q000378:metabolism*; D010588:Phagosomes / Q000201:enzymology*
chemical_list: D050505:Mutant Proteins; D003546:Cysteine Endopeptidases