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. 2020 Nov 4;10:19068. doi: 10.1038/s41598-020-76227-7

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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CVB3-induced LC3 lipidation is independent of ATG9 and WIPI2. (A,B) WIPI2 (A) and ATG9A (B) were transiently silenced in HEK293 cells through siRNA treatment for 48 h. Cells were then sham- or CVB3-infected for 16 h. Western blotting was conducted to verify the knockdown efficiency and to examine LC3 levels. Densitometric results are presented either underneath the blots or in the right panel (mean ± SD, n = 3, analyzed by one-way ANOVA with Tukey’s post-test). (C) WIPI2-KO and ATG9A-KO HEK293A cells, generated through CRISPR-Cas9 gene editing, were sham- or CVB3-infected as above, followed by western blot analysis of LC3, WIPI2, and ATG9A. Densitometry was measured and presented as above.