Figure 5
From: Erythroleukemia cells acquire an alternative mitophagy capability
The RAB9A-dependent alternative mitophagy is essential for buffering cellular stresses when canonical autophagy is abolished.
(A) Quantification analysis of the apoptosis rate in wild-type and Atg7−/− K562 cells treated with CCCP when Rab9A was knocked down. (B) Quantification analysis of the ROS level in wild-type and Atg7−/− K562 cells treated with CCCP when Rab9A was knocked down. (C) The expression of γ-H2AX detected by flow cytometry in wild-type, Atg7−/− and Atg7−/−-shRab9A K562 cells post 3 Gy ionizing radiation. (D) Comet assay of wild-type, Atg7−/−, wild-type shRab9A and Atg7−/−-shRab9A cells 1 h post 3 Gy ionizing radiation and quantification analysis of the tail length of comet assay of wild-type, Atg7−/−, wild-type shRab9A and Atg7−/−-shRab9A cells 3h post 3Gy ionizing radiation. (E) Detection of the expression of DNA damage repair related proteins (RAD50, RAD51, KU70, KU80, MRE11) and the conversion of LC3-I to LC3-II by immunoblotting in K562 cells post 3 Gy ionizing radiation.
