bims-nocaut Biomed News
on Non-canonical autophagy
Issue of 2026–04–19
two papers selected by
Quentin Frenger, University of Strasbourg
  1. TAX1BP1 targets STING1 via microautophagy and Golgiphagy to limit inflammatory signaling.
  2. LC3-linked Golgi-bypass exocytosis fortifies epithelial barrier defense.
  1. Autophagy. 2026 Apr 16. 1-3
    TAX1BP1 targets STING1 via microautophagy and Golgiphagy to limit inflammatory signaling.
    Sujit Suklabaidya, Suchitra Mohanty, Edward W Harhaj.
      The CGAS-STING1 pathway plays a key role in detecting cytosolic DNA and initiating immune responses. Excessive STING1 activation can lead to aberrant inflammation and autoinflammatory diseases; therefore, the STING1 degradation pathway is tightly regulated by several negative regulatory mechanisms. In our recent study, we show that the selective autophagy receptor TAX1BP1 functions as a negative regulator of STING1 signaling. TAX1BP1 promotes the degradation of activated STING1 through microautophagy by facilitating the interaction of STING1 with the ESCRT-0 protein HGS, and selective autophagy of the Golgi apparatus in a process known as Golgiphagy. In TAX1BP1-deficient macrophages, STING1 aggregates accumulate at the trans-Golgi network, leading to stronger antiviral and inflammatory responses. These findings support a novel mechanism linking organelle quality control and innate immune regulation, highlighting Golgiphagy as an important feedback mechanism that limits STING1 signaling.Abbreviations: cGAMP: cyclic guanosine monophosphate-adenosine monophosphate; CGAS: Cyclic GMP-AMP synthase; ER: endoplasmic reticulum; ESCRT: endosomal sorting complex required for transport; ECTV: ectromelia virus; HGS: hepatocyte growth factor-regulated tyrosine kinase substrate; IKK: IκB kinase; IRF3: interferon regulatory factor 3; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; SQSTM1: sequestosome 1; STING1: stimulator of interferon response cGAMP interactor 1; TBK1: TANK binding kinase 1; TAX1BP1: Tax1 binding protein 1.
    Keywords:  CGAS; Golgiphagy; SQSTM1/p62; STING1; TAX1BP1; microautophagy
    DOI:  https://doi.org/10.1080/15548627.2026.2658230
  2. Autophagy. 2026 Apr 12.
    LC3-linked Golgi-bypass exocytosis fortifies epithelial barrier defense.
    Jiabin Wang, Junkai Wang, Xinyu Xiao, Lingling Zheng, Xia Lu, Li Wang, Xin Bian, Long Lin.
      Cells dynamically regulate membrane protein delivery to meet physiological demands, yet how external cues rapidly mobilize unconventional Golgi-bypass exocytic routes in vivo remains unclear. Here we define LC3/Atg8-associated carrier exocytosis (LACES), a conserved program that couples microbial cues to accelerated surface delivery. In the Caenorhabditis elegans intestine, phenazine-1-carboxamide (PCN) triggers VPS-34-dependent PtdIns3P generation at ILE-1/ERGIC-53 subdomains, enabling Atg8ylation on preexisting single-membrane RAB-8 carriers. This route accelerates delivery of the ABC transporter PGP-1 and improves host survival during infection, while operating independently of the unfolded protein response, canonical macroautophagy/autophagy initiation modules, and LC3-associated phagocytosis regulators. The pathway is engaged by multiple extracellular bacteria and also functions in mammalian epithelia, where PCN increases apical ΔF508-CFTR delivery in polarized Caco-2 cysts with measurable functional improvement and enhances LC3-RAB8 interactions in mouse intestinal epithelium. These findings establish a conserved LC3-linked Golgi-bypass route and illustrate how microbial cues can rapidly rewire epithelial membrane trafficking to fortify barrier defense.
    Keywords:  Atg8ylation; LC3-linked Golgi-bypass secretion; RAB8 carriers; epithelial barrier defense; phenazine-1-carboxamide; unconventional protein secretion
    DOI:  https://doi.org/10.1080/15548627.2026.2659291
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