Fig. 6

The CS are autophagy substrates. a MCF7 cell extracts of stable CRISPR/Cas9 non-targeting control (CTRL), ATG5- or ATG7-transfected partial knock-out pools immunoblotted for CS and centrosome proteins. Vinculin is used as loading control. b Densitometric quantification of CS and centrosome protein levels relative to vinculin, represented in (a). Columns represent the mean ± SD, n = 3, ns P > 0.05 *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001, ****P ≤ 0.0001. Unpaired Student’s t-test, two-tailed. c Stable CRISPR/Cas9 non-targeting control (CTRL), ATG5- or ATG7 partial knock-out MCF7 pools immunoblotted for CS proteins. Vinculin is used as loading control. d Densitometric quantification of CS protein levels relative to vinculin, represented in (c). Columns represent the mean ± SD, n = 3, *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. Unpaired Student’s t-test, two-tailed. e–g Immunoblot of U2OS (e), MCF7 (f) or HEK293 (g) cells treated with Baf for the indicated times and immunoblotted for PCM1, CEP131, and vinculin as loading control. h Densitometric quantification of PCM1 and CEP131 immunoblots represented in (e–g). Columns represent the mean ± SD, n = 4, ns P > 0.05, *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. Unpaired Student’s t-test, two-tailed. i Colocalization of LC3B with PCM1 or CEP131 in U2OS cells after 6 h of Baf treatment. Arrows indicate examples of colocalization. j Colocalization between SSX2IP, PCM1, and mCherry-LC3B in U2OS cells treated for 6 h with 200 nM Baf. Arrows indicate examples of colocalization. Scale bars, 10 µm. Source data are provided as a Source Data file