bims-nocaut Biomed News
on Non-canonical autophagy
Issue of 2026–11–01
two papers selected by
Quentin Frenger, University of Strasbourg
  1. ATG9 and ATG2 as lipid managers at the crossroads of autophagy and extracellular vesicle secretion.
  2. USF2 deficiency enhances intracellular clearance of Salmonella Typhimurium via xenophagy and LC3-associated phagocytosis.
  1. Autophagy. 2026 Oct 31. 1-3
    ATG9 and ATG2 as lipid managers at the crossroads of autophagy and extracellular vesicle secretion.
    Asmita Singh, Carlos M Guardia.
      Macroautophagy/autophagy maintains cellular homeostasis by delivering cytoplasmic cargo to lysosomes for degradation. Autophagosome formation requires a substantial supply of phospholipids, mainly supported by the lipid scramblase ATG9A and lipid-transfer proteins ATG2A and ATG2B. Our recent study shows that loss of these proteins also alters small extracellular vesicle (sEV) secretion and composition. Cells lacking ATG9A or ATG2A/B release more sEVs during lysosomal inhibition, yet these vesicles contain less microtubule-associated protein 1A/1B-light chain 3 (LC3) and canonical autophagy cargo receptors. These changes are accompanied by impaired amphisome formation and extensive remodeling of the cellular lipidome. Our findings suggest that ATG9A and ATG2A/B coordinate membrane and cargo distribution between autophagy and endosomal secretion, raising the possibility that disrupted lipid supply to autophagosomes redirects lipids toward extracellular vesicle (EV) biogenesis.
    Keywords:  ATG2A/B; ATG9A; Amphisomes; extracellular vesicles; lipid homeostasis
    DOI:  https://doi.org/10.1080/15548627.2026.2752748
  2. Anim Cells Syst (Seoul). 2026 ;30(1): 616-629
    USF2 deficiency enhances intracellular clearance of Salmonella Typhimurium via xenophagy and LC3-associated phagocytosis.
    Junhee Kwon, Jina Jeon, Ji Won Kim, Hamin Bae, Jaebeom Kim, Young Suk Yu, Sung Hee Baek, Keun Il Kim.
      The upstream stimulatory factor 2 (USF2) is a transcription factor known as a transcriptional activator that binds to E-box motifs in gene promoters. Recently, we reported that USF2 is also a transcriptional repressor of the genes that encode lysosomes and autophagy machinery, and that its deficiency results in the elevation of autophagy. The present study was designed to determine whether the absence of USF2 is responsible for more effective protection of the host cells from bacterial infection and intracellular bacterial growth. In this context, we employed Salmonella enterica serovar Typhimurium (S. Typhimurium) as a model pathogen and monitored the changes in intracellular bacterial burden observed in the wild-type (WT) cells and USF2-deficient cells over the time course of infection. The number of intracellular bacteria increased after infection in WT cells but remained similar or decreased in USF2-deficient cells. This phenomenon was observed in various cell types, including mouse embryonic fibroblasts (MEFs), RAW264.7 macrophage-like cells, and primary bone marrow-derived macrophages (BMDMs). The phagocytosis levels were the same in WT and USF2-deficient macrophages, but the latter had a higher basal autophagy, increased lysosome abundance, and increased expression of lysosomal genes. In addition, the components of LC3-associated phagocytosis (LAP), such as LC3B and RUBICON, together with reactive oxygen species (ROS) production, were elevated in USF2-deficient macrophages. Our results demonstrated that the enhanced autophagy in non-phagocytic cells and the elevated autophagy and LAP in phagocytes both contribute to the improved clearance of intracellular pathogens in USF2-deficient cells.
    Keywords:  LAP; Salmonella Typhimurium; USF2; autophagy; xenophagy
    DOI:  https://doi.org/10.1080/19768354.2026.2721740
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