A putative link between phagocytosis-induced apoptosis and hemocyanin-derived phenoloxidase activation

Christopher J. Coates*, Tim Whalley, Michael Wyman, Jacqueline Nairn

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)

Abstract

Apoptosis and phagocytosis are crucial processes required for developmental morphogenesis, pathogen deterrence and immunomodulation in metazoans. We present data showing that amebocytes of the chelicerate, Limulus polyphemus, undergo phagocytosis-induced cell death after ingesting spores of the fungus, Beauveria bassiana, in vitro. The observed biochemical and morphological modifications associated with dying amebocytes are congruent with the hallmarks of apoptosis, including: extracellularisation of phosphatidylserine, intranucleosomal DNA fragmentation and an increase in caspase 3/7-like activities. Previous studies have demonstrated that phosphatidylserine is a putative endogenous activator of hemocyanin-derived phenoloxidase, inducing conformational changes that permit phenolic substrate access to the active site. Here, we observed extracellular hemocyanin-derived phenoloxidase activity levels increase in the presence of apoptotic amebocytes. Enzyme activity induced by phosphatidylserine or apoptotic amebocytes was reduced completely upon incubation with the phosphatidylserine binding protein, annexin V. We propose that phosphatidylserine redistributed to the outer plasma membrane of amebocytes undergoing phagocytosis-induced apoptosis could interact with hemocyanin, thus facilitating its conversion into a phenoloxidase-like enzyme, during immune challenge.

Original languageEnglish
Pages (from-to)1319-1331
Number of pages13
JournalApoptosis
Volume18
Issue number11
DOIs
Publication statusPublished - Nov 2013

Keywords

  • Phosphatidylserine
  • Apoptosis
  • Phagocytosis
  • Innate immunity
  • Limulus polyphemus
  • Damage-associated patterns
  • INNATE IMMUNE-RESPONSE
  • LIMULUS BLOOD-CELLS
  • HORSESHOE-CRAB
  • NEUTROPHIL APOPTOSIS
  • ESCHERICHIA-COLI
  • ANNEXIN-V
  • OXIDASE ACTIVATION
  • IN-VITRO
  • POLYPHEMUS
  • PHOSPHATIDYLSERINE

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