Figure 1. Recycling endosomes contribute to autophagosome formation. REs shuttle internalized cargo such as TF (not shown) with its receptor, TFR, back to the plasma membrane. Additionally, a pool of REs containing the transmembrane protein ATG9 and ULK1 are important in autophagosome formation. Blocking RE traffic by overexpressing the RAB11 effector protein TBC1D14 or inactive RAB11^N124I leads to tubulation of REs and inhibition of starvation-induced autophagy. While ULK1 remains associated with REs, ATG9 relocalizes upon starvation, possibly to recruit membrane from other sources. Meanwhile, ULK1-positive REs partially relocalize with the autophagosome marker LC3 (not shown) and the RE membrane can be integrated into forming autophagosomes leading to deposition of TF in the autophagosomal lumen.