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TRIM23 mediates cGAS-induced autophagy in anti-HSV defense
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TRIM23 mediates cGAS-induced autophagy in anti-HSV defense
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Journal Article
TRIM23 mediates cGAS-induced autophagy in anti-HSV defense
2025
Overview
The cGAS-STING pathway, well-known to elicit interferon (IFN) responses, is also a key inducer of autophagy upon virus infection or other stimuli. Whereas the mediators for cGAS-induced IFN responses are well characterized, much less is known about how cGAS elicits autophagy. Here, we report that TRIM23, a unique TRIM protein harboring both ubiquitin E3 ligase and GTPase activity, is crucial for cGAS-STING-dependent antiviral autophagy. Genetic ablation of
TRIM23
impairs autophagic control of HSV-1 infection. HSV-1 infection or cGAS-STING stimulation induces TBK1-mediated TRIM23 phosphorylation at S39, which triggers TRIM23 autoubiquitination and GTPase activity and ultimately elicits autophagy. Fibroblasts from a patient with herpes simplex encephalitis heterozygous for a dominant-negative, kinase-inactivating
TBK1
mutation fail to activate autophagy by TRIM23 and cGAS-STING. Our results thus identify the cGAS-STING-TBK1-TRIM23 axis as a key autophagy defense pathway and may stimulate new therapeutic interventions for viral or inflammatory diseases.
The cGAS-STING pathway senses cytosolic DNA to activate interferon responses, but has also been implicated in autophagy induction. Here the authors show that, during herpes simplex virus infection, cGAS-induced autophagy is mediated by TBK1-induced TRIM23 phosphorylation and downstream signaling events to assist in antiviral immunity.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/51
/ 13/89
/ 13/95
/ 14/19
/ 38/39
/ 49/109
/ 49/88
/ 64/110
/ 82/29
/ 82/58
/ 82/80
/ Ablation
/ Animals
/ Herpesvirus 1, Human - immunology
/ Herpesvirus 1, Human - physiology
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ Membrane Proteins - genetics
/ Membrane Proteins - metabolism
/ Mice
/ Nucleotidyltransferases - genetics
/ Nucleotidyltransferases - immunology
/ Nucleotidyltransferases - metabolism
/ Protein Serine-Threonine Kinases - genetics
/ Protein Serine-Threonine Kinases - metabolism
/ Science
/ Ubiquitin-Protein Ligases - genetics
