Citation

Rivers DB, Uçkan F, Ergin E, Keefer DA. J. Insect Physiol. 2010; 56(12): 1935-1948.

Affiliation

Department of Biology, Loyola University Maryland, Baltimore, MD USA.

Copyright

(Copyright © 2010, Elsevier Publishing)

DOI

10.1016/j.jinsphys.2010.08.019

PMID

20804763

Abstract

The ectoparasitic wasp Nasonia vitripennis produces a proteinaceous venom that induces death in fly hosts by non-paralytic mechanisms. Previous in vitro assays have suggested that the primary cause of cell and tissue death is oncosis, a non-programmed cell death (PCD) pathway characterized by cellular swelling and lysis. However, ultrastructural analyses of BTI-TN-5B1 cells exposed to LC(99) doses of wasp venom revealed cellular changes more consistent with apoptosis and/or non-apoptotic PCD than oncosis or necrosis: By 3h after incubation with venom, susceptible cells displayed indentations in the nuclear membranes, large nucleoli, and extensive vacuolization throughout the cytoplasm. In the vast majority of venom treated cells, annexin V bound to the plasma membrane surface within 15min after treatment, a characteristic consistent with translocation of phosphatidylserine to the cell surface during the early stages of apoptosis. Likewise, mitochondrial transmembrane potential was depressed in cells within 15min in venom-treated cells, an event that occurred in the absence of mitochondrial swelling or rupturing of cristae. Active caspase 3 was detected by fluorescent labelling in nearly all venom treated cells 3h after exposure to venom, and in turn, the potent caspase 3 inhibitor Z-VAD-FMK attenuated the morphological changes elicited by wasp venom and afforded protection to BTI-TN-5B1-4 cells.

Language: en