Golgi Apparatus: An Emerging Platform for Innate Immunity.

The Golgi apparatus serves as a receiving station where proteins from the endoplasmic reticulum (ER) are further processed before being sent to other cellular compartments. In addition to its well-appreciated roles in vesicular trafficking and protein/lipid secretion, recent studies have demonstrated that the Golgi acts as a signaling platform to facilitate multiple innate immune pathways. Moreover, the membranous networks that connect the Golgi with the ER, mitochondria, endosomes, and autophagosomes provide convenient access to innate immune signal transduction and subsequent effector responses. Here, we review the emerging knowledge about the roles of the Golgi in the initiation and activation of innate immune signaling. Moreover, microbial hijacking strategies that inhibit Golgi-associated innate immune responses will also be discussed. The Golgi apparatus not only functions as an inert sorting organelle but also acts as a signaling platform to facilitate innate immunity. Golgi dispersion acts as a crucial event to initiate NLRP3 inflammasome assembly, and the interface between the Golgi, ER, and mitochondria functions as an important hub for NLRP3 inflammasome activation. ER-to-Golgi trafficking of stimulator of interferon genes (STING) is required for interferon (IFN)-I production and autophagosome formation in response to cytosolic DNA or DNA viruses. The Golgi apparatus acts as the platform for TANK binding kinase 1 (TBK1) activation after Toll-like receptor (TLR)3 or retinoic acid-inducible gene I (RIG-I)-like receptors (RLR) activation. Golgi-localized IFN-inducible GTPases target intracellular pathogens either at the Golgi apparatus or after moving to other cellular compartments. A number of microorganisms use several virulence factors to counteract host defense by targeting the Golgi apparatus or Golgi-associated proteins. [ABSTRACT FROM AUTHOR]