{
  "id": 14984298,
  "title": "The Salmonella effector SspH2 disrupts F-actin cytoskeletal organization to inhibit macrophage migration",
  "url": "https://urgent.news/2026/10/16/the-salmonella-effector-ssph2-disrupts-f-actin-cytoskeletal",
  "topic": "science",
  "section": "Science",
  "published": "2026-10-16T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.10.14.759247v1?rss=1"
  },
  "original_language": "en",
  "account": "Salmonella enterica serovar Typhimurium, a pathogen that causes gastroenteritis in humans and persistent infections in animals, harbors a variety of type III secretion system effectors within Salmonella Pathogenicity Island 2 (SPI-2). One such effector, SspH2, is an E3 ubiquitin ligase that inhibits host cell migration. However, the mechanism by which SspH2 achieves this remains unclear. Researchers employed time-lapse microscopy and wound-healing assays to investigate SspH2's role in suppressing macrophage-like RAW264.7 cells' movement.\n\nUpon SspH2 expression, a significant reduction in F-actin and a decreased number of cells possessing higher-order F-actin structures were observed, suggesting cytoskeletal remodeling. The catalytically inactive mutant SspH2C580A, lacking E3 ligase activity, did not exhibit any effect on cell movement, confirming the essential role of E3 ligase activity in SspH2's inhibitory effects. Interestingly, knockdown of vinculin, a crucial component of podosomes and focal adhesions, replicated SspH2's impact on cell migration. When vinculin expression was diminished, SspH2 no longer inhibited migration, indicating that SspH2 requires vinculin-associated F-actin-rich structures to impede cell movement.\n\nThese findings reveal a novel pathway employed by Salmonella Typhimurium to limit host cell movement, potentially contributing to immune evasion and the bacterium's fitness within the host.",
  "summary": "The facultative intracellular pathogen Salmonella enterica serovar Typhimurium (S. Typhimurium) causes gastroenteritis in humans and persistent infections in animals, enabling widespread environmental reservoirs. Intracellular survival of S. Typhimurium depends on a suite of type III secretion system effectors encoded within Salmonella Pathogenicity Island 2 (SPI-2), many of which also impair…",
  "key_points": [],
  "editors_take": null,
  "illustration": null,
  "coverage": {
    "outlets": 1,
    "also_reported_by": []
  },
  "ai_generated": true,
  "disclaimer": "Summaries, key points and the editor’s take are written by software from other outlets’ reporting and may contain errors — always check the linked original."
}