Skip to content
DraconiticResearch
Search Sources API
209,932 studies31 sourcesUpdated 8 min ago
Peer-reviewedCC BY-NC-ND 4.0Scientific Reports

Host CD59 potentiates the type III secretion system in Yersinia pseudotuberculosis

  • Kristen J. Davis1,2
  • Kerri-Lynn Sheahan1,3,4
  • Connor S. Murphy1,3,5
  • Joshua J. Whiteley6
  • Bree B. Aldridge1,3,6
  • Ralph R. Isberg1,3
6 affiliations
  1. 1Department of Molecular Biology and Microbiology, Tufts University Graduate School of Biomedical Sciences, Boston, MA USA
  2. 2Graduate Program in Molecular Microbiology, Tufts University Graduate School of Biomedical Sciences, Boston, MA USA
  3. 3Tufts University School of Medicine, Boston, MA USA
  4. 4Present Address: Obsidian Therapeutics, Cambridge, MA USA
  5. 5Present Address: Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, ME USA
  6. 6Tufts University School of Engineering, Medford, MA USA
Read full textPDFDOICite

Abstract

Type III secretion systems (T3SS) play critical roles in disease for many Gram-negative pathogens. Although the structural details of T3SS assembly have been extensively studied, the intimate interactions between T3SS components and the target host plasma membrane are poorly characterized. A previous RNA interference (RNAi) study identified the GPI-linked surface protein CD59 as a critical host component that supports the translocation of Yersinia pseudotuberculosis (Yptb) T3SS effectors into the host cytosol. We show here that both depletion and increased levels of CD59 reduced Yptb T3SS pore formation and Yop translocation into host target cells. CD59 is unlikely to act as a receptor for the T3SS translocon, as physical blockade of CD59 or enzymatic removal of all GPI-linked surface proteins had no effect on T3SS function. Consistent with its importance in supporting T3SS function, efficient bacterial effector-mediated focal adhesion disassembly was dependent on CD59. Surprisingly, depletion of CD59 interfered with the rearrangement of the lipid raft marker GM1 that occurs after Yptb adhesion to host cells, indicating that CD59 supports lipid microdomain dynamics. Consistent with a role in modulating lipid composition, the loss of CD59 led to the accumulation of phosphatidylcholine and alterations in both fatty acid chain lengths and saturation levels. This work points to a role for CD59 in maintaining plasma membrane dynamics necessary for efficient T3SS translocon function. In addition, a polarization index is described that quantifies the asymmetric association of membrane compartments with organelles.

Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1038/s41598-026-65480-x.

Related

  1. 6-Gingerol Potentiates β-Cell Insulin Secretion Without Acting as an L-Cell GLP-1 Secretagogue
    Vilasinee Intisang, Piyathida Yameephai, Kwanchanok Uppakara +1
    International Journal of Molecular SciencesPeer-reviewedCC BY 4.0Full textSurgery & anaesthesiaCrossrefEurope PMC
  2. From gut colonization to recurrence: E. coli secretion systems at the host-microbiota interface.
    Marcin Równicki, Maciej Obrębski, Jakub P Piwowarski
    Gut microbesPeer-reviewedCC BYFull textEndocrinology & metabolismEurope PMC
  3. The Central Melanocortin System Regulates Growth Hormone Secretion
    Ligia M. M. de Sousa, Vanielle A. do N. Vicente, Guilherme A. Alves +3
    The Journal of NeurosciencePeer-reviewedPublisher termsFull textPhysiologyPMC
  4. The ESX-2 type VII secretion system is required for Mycobacterium tuberculosis survival under nutrient starvation and for reactivation from dormancy
    Camilla Vullo, Mariagrazia Di Luca, Cosmeri Rizzato +9
    Microbiology SpectrumPeer-reviewedCC BY 4.0Full textInfectious diseaseHAL
  5. Liver abscess complicated by sepsis due to Yersinia enterocolitica: a case report
    Huanhuan Lin, Yuxiang Liu, Peng Ding +3
    Frontiers in medicinePeer-reviewedCC BYFull textGeneral medicineEurope PMC

Cite

BibTeXRIS
BibTeX
@article{davis2026host,
  title = {{Host CD59 potentiates the type III secretion system in Yersinia pseudotuberculosis}},
  author = {Kristen J. Davis and Kerri-Lynn Sheahan and Connor S. Murphy and Joshua J. Whiteley and Bree B. Aldridge and Ralph R. Isberg},
  journal = {Scientific Reports},
  year = {2026},
  month = aug,
  doi = {10.1038/s41598-026-65480-x},
  url = {https://doi.org/10.1038/s41598-026-65480-x},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Host CD59 potentiates the type III secretion system in Yersinia pseudotuberculosis
AU  - Kristen J. Davis
AU  - Kerri-Lynn Sheahan
AU  - Connor S. Murphy
AU  - Joshua J. Whiteley
AU  - Bree B. Aldridge
AU  - Ralph R. Isberg
PY  - 2026
DA  - 2026/08/08
JO  - Scientific Reports
DO  - 10.1038/s41598-026-65480-x
UR  - https://doi.org/10.1038/s41598-026-65480-x
AB  - Type III secretion systems (T3SS) play critical roles in disease for many Gram-negative pathogens. Although the structural details of T3SS assembly have been extensively studied, the intimate interactions between T3SS components and the target host plasma membrane are poorly characterized. A previous RNA interference (RNAi) study identified the GPI-linked surface protein CD59 as a critical host component that supports the translocation of Yersinia pseudotuberculosis (Yptb) T3SS effectors into the host cytosol. We show here that both depletion and increased levels of CD59 reduced Yptb T3SS pore formation and Yop translocation into host target cells. CD59 is unlikely to act as a receptor for the T3SS translocon, as physical blockade of CD59 or enzymatic removal of all GPI-linked surface proteins had no effect on T3SS function. Consistent with its importance in supporting T3SS function, efficient bacterial effector-mediated focal adhesion disassembly was dependent on CD59. Surprisingly, depletion of CD59 interfered with the rearrangement of the lipid raft marker GM1 that occurs after Yptb adhesion to host cells, indicating that CD59 supports lipid microdomain dynamics. Consistent with a role in modulating lipid composition, the loss of CD59 led to the accumulation of phosphatidylcholine and alterations in both fatty acid chain lengths and saturation levels. This work points to a role for CD59 in maintaining plasma membrane dynamics necessary for efficient T3SS translocon function. In addition, a polarization index is described that quantifies the asymmetric association of membrane compartments with organelles.  Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1038/s41598-026-65480-x.
SN  - 2045-2322
ER  -