Autophagy is a conserved cellular process in eukaryotes that functions as a cellular garbage disposal system. During starvation or other cellular stresses, all cells are able to eat its own parts and recycle them. Autophagy degrades of misfolded proteins, long-lived proteins and damaged organelles by sequestering them in a double-membraned vesicle and fusing this vesicle with the lysosome for degradation. Autophagy dysfunction can lead to certain types of cancer, neurodegenerative disorders, immunological disorders, development, cellular ageing and cell death.

In humans, autophagy is regulated by AuTophagy related Gene proteins (Atg proteins). Atg5-Atg12-Atg16 complex facilitates the lipidation of LC3 family proteins. LC3 interacts with autophagy related proteins through LIR (LC3 Interacting Region) residues. So far, no LIR region has been reported on Atg16L1. For the first time we demonstrate the mode of interaction of LC3 family proteins with Atg16L1.