MAP1LC3C

Autophagy is a highly regulated bulk degradation process that plays an important role in cellular maintenance and development. MAP1LC3C is an ortholog of the yeast autophagosome protein Atg8 (He et al., 2003 [PubMed 12740394]).[supplied by OMIM, Nov 2010]

Full Name

Microtubule Associated Protein 1 Light Chain 3 Gamma

Function

Ubiquitin-like modifier that plays a crucial role in antibacterial autophagy (xenophagy) through the selective binding of CALCOCO2 (PubMed:23022382).
Recruits all ATG8 family members to infecting bacteria such as S.typhimurium (PubMed:23022382).
May also play a role in aggrephagy, the macroautophagic degradation of ubiquitinated and aggregated proteins (PubMed:28404643).

Biological Process

AggrephagyManual Assertion Based On ExperimentIMP:UniProtKB
Autophagosome assemblyManual Assertion Based On ExperimentIBA:GO_Central
Autophagosome maturationManual Assertion Based On ExperimentIDA:UniProtKB
Autophagy of mitochondrionManual Assertion Based On ExperimentIBA:GO_Central
Cellular response to nitrogen starvationManual Assertion Based On ExperimentIBA:GO_Central
Cellular response to starvationManual Assertion Based On ExperimentIDA:UniProtKB
MacroautophagyManual Assertion Based On ExperimentIDA:UniProtKB
Protein exit from endoplasmic reticulumManual Assertion Based On ExperimentIMP:CACAO

Cellular Location

Cytoplasmic vesicle, autophagosome membrane
Endomembrane system
Cytoplasm, cytoskeleton
LC3-II binds to the autophagic membranes.

PTM

The precursor molecule is cleaved by ATG4 (ATG4A, ATG4B, ATG4C or ATG4D) to expose the glycine at the C-terminus and form the cytosolic form, LC3-I (PubMed:15187094, PubMed:20818167, PubMed:30661429, PubMed:31709703).
The processed form is then activated by APG7L/ATG7, transferred to ATG3 and conjugated to phosphatidylethanolamine (PE) phospholipid to form the membrane-bound form, LC3-II (PubMed:15187094).
During non-canonical autophagy, the processed form is conjugated to phosphatidylserine (PS) phospholipid (PubMed:33909989).
ATG4 proteins also mediate the delipidation of PE-conjugated forms (PubMed:33909989, PubMed:31709703).
In addition, ATG4B and ATG4D mediate delipidation of ATG8 proteins conjugated to PS during non-canonical autophagy (PubMed:33909989).
(Microbial infection) The Legionella effector RavZ is a deconjugating enzyme that hydrolyzes the amide bond between the C-terminal glycine residue and an adjacent aromatic residue in ATG8 proteins conjugated to phosphatidylethanolamine (PE), producing an ATG8 protein that is resistant to reconjugation by the host machinery due to the cleavage of the reactive C-terminal glycine (PubMed:23112293, PubMed:31722778).
RavZ is also able to mediate delipidation of ATG8 proteins conjugated to phosphatidylserine (PS) (PubMed:33909989).
Phosphorylation at Ser-96 and Ser-98 by TBK1 prevents interaction with ATG4 (ATG4A, ATG4B, ATG4C or ATG4D) (PubMed:31709703).
Phosphorylation by TBK1 on autophagosomes prevents their delipidation by ATG4 and premature removal from nascent autophagosomes (PubMed:31709703).