Signaling inputs into the systems regulating atg8ylation and canonical autophagy. To underscore that atg8ylation apparatus can act independently of canonical autophagy, the system is split into two parts (A and B). Atg8ylation E3 ligase centered upon ATG16L1 (A; see Fig. 1) and the FIP200 complex (B). For canonical autophagy, A and B come together (see Fig. 2). Three types of major inputs affecting components A or B or both are in peach-colored boxes (I–III) and fall in three categories: immune signals (I), signals coming from selective autophagy receptors (II), and metabolic signals (III). Immune signals are collected via PRRs assisted in many cases by immunity-related GTPases such as IRGM and often (but not exclusively) transduced via TBK1 to several components controlling atg8ylation and canonical autophagy apparatus. Cargo recognition by SLRs relays cargo capture, whereas SLRs can associate with FIP200 and in turn receive further signals from TBK1. Note that the ATG16L1 E3 ligase participates in FIP200 complex–independent standalone atg8ylation processes such as LAP and others (categorized in Fig. 1). Details in the text.