Selective Autophagy Controls Innate Immune Response Through a Tak1/Tab2/Sh3px1 Axis

Selective autophagy is a catabolic route which turns over specific cellular material for degradation by lysosomes, and whose role in the regulation of innate immunity largely unexplored. Here, we show that apical kinase Drosophila immune deficiency (Imd) pathway Tak1, as well its co-activator Tab2, are both novel selective substrates interact with protein Atg8a. We also Atg8a-interacting Sh3px1 downregulation Imd pathway, facilitating targeting Tak1/Tab2 complex to platform through interaction Tab2. Our findings Tak1/Tab2/Sh3px1 interactions Atg8a mediate autophagic complex, turn prevents constitutive activation Drosophila. This study provides mechanistic insight on responses autophagy.