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ARS Home » Northeast Area » Orono, Maine » National Cold Water Marine Aquaculture Center » Research » Publications at this Location » Publication #371592
Title: Mechanisms of eastern oyster, Crassostrea Virginica, hemocyte apoptosis in response to infection with Perkinsus Marinus

Author
item ROBERTS, ERIN - University Of Rhode Island
item WICKFORS, GARY - National Oceanic & Atmospheric Administration (NOAA)
item Proestou, Dina
item Markey Lundgren, Kathryn
item SULLIVAN, MARY - University Of Rhode Island
item GOMEZ-CHIARRI, MARTA - University Of Rhode Island

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 12/13/2019
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Apoptosis, or programmed cell death, of hemocytes may be a critical step in oyster immune defense against Perkinsus marinus infection in the eastern oyster. Increased hemocyte apoptosis may prevent or reduce P. marinus replication in infected individuals. The precise apoptotic pathway and molecules involved in response to intracellular infection with P. marinus are poorly understood. To investigate which apoptotic pathways are involved in hemocyte response to P. marinus, eastern oysters bred for high survival in the Chesapeake Bay were challenged in vivo with P. marinus. Hemocyte apoptosis, caspase 3/7 activation, and lysosomal permeabilization were investigated 7 days post-infection using flow cytometry. Granular hemocyte apoptosis significantly decreased in challenged oysters, indicating possible inhibition by the parasite. Caspase 3/7 activation and lysosomal permeabilization were not significantly affected by P. marinus challenge, indicating likely involvement of a caspase-independent pathway in hemocyte response. Gene expression analysis also revealed increased expression of mitochondrial pathway molecules. To investigate direct functional involvement of the mitochondrial pathway of apoptosis, oyster hemocytes were challenged in vitro with P. marinus at four multiplicities of infection (P. marinus to hemocyte 1:1, 5:1, 10:1, and 25:1). The levels of apoptosis and mitochondrial permeabilization, a marker of the mitochondrial pathway, were measured one hour post-challenge using flow cytometry. Results will inform future experiments inhibiting the mitochondrial pathway of apoptosis following Dermo challenge. Understanding apoptotic pathways involved in Dermo disease response may aid in targeting genes for breeding for disease resistance.