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Autophagy is a conserved cell-survival membrane trafficking pathway implicated in pathologies such as cancer.Much is still unknown about how autophagy is regulated in particular from intracellular compartments such as the Golgi complex.WAC was discovered in our genome-wide screen to be an positive regulator of autophagy (McKnight et al., 2012).WAC is in the nucleus and on the Golgi, where it affects transcription and Golgi biogenesis respectively (Totsukawa et al., 2011;Zhang and Yu, 2011).We aim to understand the mechanism behind WACs regulation of autophagy and how WAC itself is regulated.We hypothesise WAC is affecting autophagy through its nuclear and cytoplasmic functions.We have investigated: Atg9 Iocalisation, ULK1 signalling, LC3 lipidation, p62 degradation, LC3B and WIPI2 puncta formation.This has confirmed that WAC is a positive regulator of autophagy that acts early on in the pathway.Moreover, reintroduction of WAC into WAC-depleted cells rescues WIPI2 and LC3B puncta formation, two markers for autophagosomal structures.Cytoplasmic binding partners of WAC have been investigated by mass spectrometry and revealed an interaction with a golgi tethering protein.Knockdown and rescue experiments suggest this tether acts as a receptor for WAC on the Golgi, and the interaction is enhanced upon starvation.Additional data on the regulation of WAC and trafficking to the autophagosome will be presented.