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Figure 8


Fig. 8. Model of subcellular Atg9 trafficking in S. cerevisiae. (A) Atg9 cycles between the PAS and mitochondria. Atg9 sorting from mitochondria is blocked by disruption of the ER-mitochondrial network by early sec mutations, deletion mutants that lack VFT-complex subunit and actin filament disruption. Once the double-membrane vesicle is completed and the function of Atg9 is no longer needed, the Atg1-Atg13 complex triggers the retrieval transport of this protein from the PAS (Reggiori et al., 2004a). Atg2, Atg18 and the PtdIns(3)P generated by the Atg14-containing PtdIns 3-kinase complex I also participate in this recycling event. (B) Inhibition of the Atg9 sorting event from mitochondria. The proper organization of the mitochondrial reticulum is maintained by both the cytoskeleton and a direct connection with the ER. Alteration of one of these structures provokes the disruption of the mitochondrial network, which blocks Atg9 trafficking. LatA treatment and deletion of each one of the subunits of the VFT complex affects actin filaments, whereas early sec mutations disrupt the ER peripheral network. In addition, actin also plays a direct role in Atg9 delivery and cargo recruitment to the PAS (Reggiori et al., 2005a).





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