STING (stimulator of interferon genes) is a central molecule that binds to cyclic dinucleotides produced by the cyclic GMP-AMP synthase (cGAS) to activate innate immunity against microbial infection. Here we report that STING harbors classic LC-3 interacting regions (LIRs) and mediates autophagy through its direct interaction with LC3. We observed that poly(dA: dT), cGAMP, and HSV-1 induced STING-dependent autophagy and degradation of STING immediately after TBK1 activation. STING induces non-canonical autophagy that is dependent on ATG5, whereas other autophagy regulators such as Beclin1, Atg9a, ULK1, and p62 are dispensable. LIR mutants of STING abolished its interaction with LC3 and its activation of autophagy. Also, mutants that abolish STING dimerization and cGAMP-binding diminished the STING-LC3 interaction and subsequent autophagy, suggesting that STING activation is indispensable for autophagy induction. Our results thus uncover dual functions of STING in activating the immune response and autophagy, and suggest that STING is involved in ensuring a measured innate immune response.

Nanometer-sized particles that are well dispersed in a polymer melt, presumably due to strongly favorable particle−polymer interactions, can form fractal structures via polymer bridging, leading ultimately to a nanoparticle (NP) network analogous to a colloidal gel. The linear viscoelastic response of polymer nanocomposites can be quantitatively predicted by a parameter-free model in which the stress is a simple sum of contributions from the polymer matrix and the fractal NP structure linked by bridging polymer chains. The NP contribution is modeled using critical percolation, while the polymer part is enhanced by the presence of particles, owing to hydrodynamic interactions. The phase diagram at the right shows that small NPs are needed to achieve the stronger reinforcement from glassy bridges at reasonable particle loadings.