bioRxivJClub
P. aeruginosa disrupts ARP-2/3 mediated apical F-actin organization to induce intestinal deformation in C. elegans
bioRxiv · · Preprint · Open access
Divyashree, Sinha + 1 more
Abstract ↗AI summary
The abstract is read at the publisher; the summary is JClub's.
Heat-labile factors secreted by Pseudomonas aeruginosa disrupt apical polarity in Caenorhabditis elegans enterocytes, causing apical F-actin fragmentation, F-actin-rich vesicles, and pronounced apical surface deformation.
- Why it matters: In-vitro monolayers miss multicellular tissue mechanics, leaving unclear how extracellular bacterial signals remodel host polarity–cytoskeleton coupling during infection.
- What they did: The study used C. elegans infection to show PI3K-AKT-dependent apical enrichment of PI(3,4,5)P3, ARP-2/3 fragmentation, localized apical F-actin disruption, and lumenal release of F-actin-rich vesicles.
- The result: Disrupting CDC-42–ARP-2/3 actin assembly, PI3K-AKT signaling, or endotube regulators IFB-2 and IFO-1 suppressed intestinal deformation and significantly extended host survival without detectable epithelial tissue integrity loss.
The findingWhy it mattersWhat they didThe result
- Open access