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. 2011 Apr 5;30(11):2101–2114. doi: 10.1038/emboj.2011.104

Figure 6.

Figure 6

Mitochondrial respiratory deficiency impairs PAS recruitment of the Atg1–Atg13 complex under amino-acid starvation. (A) ATG8 induction is independent of the Atg1–Atg13 complex and autophagic flux. Wild-type, rho0, Δatg1, Δatg7, Δatg9, and Δatg11 cells harbouring prATG8-GFP-ATG8 were analysed as described in Figure 1A. The means and s.d. of four (n=4) independent experiments are indicated. (B) Atg1 and Atg13 recruitment to the PAS depends on mitochondrial function. Wild-type and rho0 cells harbouring prATG8-GFP-ATG8 and prATG1-ATG1-mCherry (upper panels) or prATG13-ATG13-mCherry (lower panels) were exposed to amino-acid starvation medium supplemented with galactose for 3 h. Wild-type cells were treated with antimycin A (AA 30′) after 2.5 h of starvation for 30 min or with oligomycin (O) for 3 h of starvation. Arrowheads indicate the position of GFP-Atg8 puncta. Transmission and fluorescence light microscopy images were superimposed to visualize cellular boundaries. Scale bar represents 1.5 μm. (C) Steady-state levels of Atg1- and Atg13-mCherry during amino-acid starvation. Wild-type, rho0, and Δatg7 cells expressing prATG1-ATG1-mCherry (upper panels) or prATG13-ATG13-mCherry (lower panels) were exposed and treated as described in (B) and analysed by whole cell extraction and western blot analysis using α-dsRed and α-Cdc11 antibodies.