Xiong, QiuhongÜnal, Can MuratMatthias, JanSteinert, MichaelEichinger, Ludwig2021-01-082021-01-0820152046-2441http://doi.org/10.1098/rsob.150008https://hdl.handle.net/20.500.12846/288Unal, Can/0000-0003-4710-9567; Eichinger, Ludwig/0000-0003-1594-6117WOS:000355309700004PubMed: 25878144Macroautophagy is a highly conserved intracellular bulk degradation system of all eukaryotic cells. It is governed by a large number of autophagy proteins (ATGs) and is crucial for many cellular processes. Here, we describe the phenotypes of Dictyostelium discoideum ATG160(-) and ATG9(-)/16(-) cells and compare them to the previously reported ATG9(-) mutant. ATG16 deficiency caused an increase in the expression of several core autophagy genes, among them atg9 and the two atg8 paralogues. The single and double ATG9 and ATG16 knock-out mutants had complex phenotypes and displayed severe and comparable defects in pinocytosis and phagocytosis. Uptake of Legionella pneumophila was reduced. In addition, ATG9(-) and ATG16(-) cells had dramatic defects in autophagy, development and proteasomal activity which were much more severe in the ATG9(-)/16(-) double mutant. Mutant cells showed an increase in poly-ubiquitinated proteins and contained large ubiqui-tin-positive protein aggregates which partially co-localized with ATG16-GFP in ATG9(-)/16(-) cells. The more severe autophagic, developmental and proteasomal phenotypes of ATG9(-)/16(-) cells imply that ATG9 and ATG16 probably function in parallel in autophagy and have in addition autophagy-independent functions in further cellular processes.eninfo:eu-repo/semantics/openAccessDictyosteliumAutophagyDevelopmentPhagocytosisProteasomeProtein AggregateArticle5410.1098/rsob.150008Q1Q1WOS:0003553097000042-s2.0-84935025281