LGG-1/GABARAP lipidation is dispensable for autophagy and development in C .elegans

The ubiquitin-like proteins Atg8/LC3/GABARAP are required for multiple steps of autophagy such as initiation, cargo recognition and engulfment, vesicle closure and degradation. Most of LC3/GABARAP functions are considered dependent on their post-translational modifications and addressing to membranes through a conjugation to a lipid, the phosphatidylethanolamine. Contrarily to mammals, C. elegans possesses single homologs of LC3 and GABARAP families, named LGG-2 and LGG-1. Using site directed mutagenesis, we inhibited the conjugation of LGG-1 to the autophagosomal membrane and generated mutants that express only cytosolic forms, either the precursor or the cleaved protein. LGG-1 is an essential gene for autophagy and development in C. elegans , but we discovered that its functions could be fully achieved independently of its localization to the membrane. This study reveals an essential role for the cleaved form of LGG-1 in autophagy but also in an autophagy independent embryonic function. Our data question the use of the lipidated GABARAP/LC3 as the main marker of autophagic flux and highlight the high plasticity of autophagy.