Article title: Autophagy inhibition promotes defective neosynthesized proteins storage in ALIS, and induces redirection toward proteasome processing and MHCI-restricted presentation
Authors: Till Wenger, Seigo Terawaki, Voahirana Camosseto, Ronza Abdelrassoul, Anna Mies, Nadia Catalan, Nuno Claudio, Giovanna Clavarino, Aude de Gassart, Francesca de Angelis Rigotti, Evelina Gatti, and Philippe Pierre
Journal: Autophagy
Bibliometrics: Volume 8, Issue 3, Pages 350–63
DOI: 10.4161/auto.18806
It has come to our attention that two of the microscopy panels in Figure 1B and C in the original version of this article were duplicated in error. This duplication did not change the overall interpretation of the figures nor the conclusion of the paper. The original staining for SQSTM1/p62 in HeLa cells treated with 3MA that was missing in Figure 1B are provided below:
Figure 1.
ALIS form upon autophagy inhibition, and differ from proteasome inhibition induced aggregates. (A) HeLa cells were treated for 4 h with 3-MA (5mM) or left untreated (control) and stained for polyubiquitinated proteins (FK1 antibody, polyUbi, green), NBR1 (red) and p62 (blue) prior to analysis by confocal microscopy. (B) HeLa cells were treated for 4h with 3-MA (5 mM), Puromycin (5 μg/ml) or Epoxomycin (5 μM). Cells were stained for ubiquitinated protein (FK2 antibody, polyUbi, blue), Hsc70 (green), and p62 (red). Arrowheads indicate ALIS in the overlay and the corresponding area in the Hsc70 staining, respectively. Pearson's coefficient (R) is given for the colocalization of p62 and Hsc70. (C) HeLa cells were transfected with siRNA against ATG5 (siATG5) or control siRNA (siCo) and stained for ubiquitinated protein (FK2 antibody, polyUbi, blue), HSC70 (green), and p62 (red). Bar, 10 μm.
The authors apologize for any inconvenience caused.