ATG16L1
ATG16L1 (autophagy related 16 like 1, also known as WDR30, ATG16A and APG16L) is a WD repeat protein that works with ATG12-ATG5 to drive ATG8 lipidation. It acts in both canonical and non-canonical autophagy, the pathways that deliver intracellular components to lysosomes. Browse Assay Genie's current range of ATG16L1 research reagents below, or read on for the biology behind the target.
ATG16L1 is an essential component of the autophagy machinery. In canonical autophagy it interacts with ATG12-ATG5 to mediate the conjugation of phosphatidylethanolamine (PE) to ATG8 family proteins, including MAP1LC3A, MAP1LC3B, MAP1LC3C, GABARAP, GABARAPL1 and GABARAPL2. This produces a membrane-bound, activated form of ATG8 and controls elongation of the nascent autophagosomal membrane. The protein acts as a molecular hub, with distinct domains supporting either canonical or non-canonical signalling.
In non-canonical autophagy, ATG8 proteins are conjugated to single membranes at endolysosomal compartments, probably through conjugation of phosphatidylserine (PS). This pathway helps epithelial cells limit lethal infection by influenza A virus. As part of the ATG8 conjugation system with ATG5 and ATG12, ATG16L1 is also required to recruit LRRK2 to stressed lysosomes and to induce LRRK2 kinase activity in response to lysosomal stress. It regulates mitochondrial antiviral signalling (MAVS)-dependent type I interferon production and negatively regulates NOD1- and NOD2-driven inflammatory cytokine responses. Together with NOD1 or NOD2, it promotes an autophagy-dependent antibacterial pathway. It also has a role in the morphology and function of Paneth cells.
The ATG16L1 gene belongs to the HGNC groups for WD repeat domain containing and autophagy related genes, and the protein belongs to the WD repeat ATG16 family. Its UniProt locations include the cytoplasm, preautophagosomal structure membrane, endosome membrane and lysosome membrane. Defects in the gene are a cause of susceptibility to inflammatory bowel disease type 10 (IBD10), and several transcript variants encoding different isoforms have been described. Earlier names refer to the yeast ATG16 and APG16 homologues.
ATG16L1 pairs with ATG12-ATG5 to lipidate ATG8 proteins and control elongation of the nascent autophagosomal membrane.
It supports ATG8 conjugation to single endolysosomal membranes, a pathway that helps epithelial cells limit lethal influenza A infection.
ATG16L1 regulates MAVS-dependent interferon production, restrains NOD1 and NOD2 cytokine responses and promotes an autophagy-dependent antibacterial pathway.
Defects in the gene confer susceptibility to inflammatory bowel disease type 10, and the protein influences Paneth cell morphology and function.
ATG16L1 interacts with ATG12-ATG5 to mediate conjugation of phosphatidylethanolamine to ATG8 family proteins, which controls autophagosomal membrane elongation. It also functions in non-canonical autophagy at endolysosomal membranes and in lysosomal stress responses involving LRRK2.
ATG16L1 is also called WDR30, FLJ10035, ATG16A, APG16L and ATG16L. Earlier HGNC names describe it as an S. cerevisiae APG16 or ATG16 autophagy 16-like gene. UniProt lists the protein as autophagy-related protein 16-1. Several transcript variants encode different isoforms.
Defects in the ATG16L1 gene are a cause of susceptibility to inflammatory bowel disease type 10 (IBD10). A mouse ortholog, Atg16l1, exists, so researchers can study it in mouse models. Check the datasheet of any product for its validated reactivity.
Other autophagy-related proteins, including the ATG12-ATG5 conjugation partners and components of the ATG8 lipidation system.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q676U5; product specifications from Assay Genie datasheets.