Autophagy is an intracellular bulk protein degradation system. Beclin is kn
own to be involved in this process; however, its role is unclear. In this s
tudy, we showed that Beclin was co-immunoprecipitated with phosphatidylinos
itol (PtdIns) 3-kinase, which is also required for autophagy, suggesting th
at Beclin is a component of the PtdIns 3-kinase complex. Quantitative analy
ses using a cross-linker showed that all Beclin forms a complex with PtdIns
3-kinase, whereas similar to 50% of PtdIns 3-kinase remains free from Becl
in. Indirect immunofluorescence microscopy demonstrated that the majority o
f Beclin and PtdIns 3-kinase localize to the trans-Golgi network (TGN). Som
e PtdIns 3-kinase is also distributed in the late endosome. These results s
uggest that Beclin and PtdIns 3-kinase control autophagy as a complex at th
e TGN.