FN Archimer Export Format
PT J
TI Molecular and cellular characterization of apoptosis in flat oyster a key mechanisms at the heart of host-parasite interactions
BT 
AF GERVAIS, Ophelie
   RENAULT, Tristan
   ARZUL, Isabelle
AS 1:1;2:2;3:1;
FF 1:PDG-RBE-SGMM-LGPMM;2:PDG-RBE;3:PDG-RBE-SGMM-LGPMM;
C1 Ifremer, Stn La Tremblade, RBE LGPMM SG2M, Ave Mus Loup, F-17390 La Tremblade, France.
   Ifremer, Ctr Nantes, RBE, Rue Ile dYeu, Nantes, France.
C2 IFREMER, FRANCE
   IFREMER, FRANCE
SI LA TREMBLADE
   NANTES
SE PDG-RBE-SGMM-LGPMM
   PDG-RBE
IN WOS Ifremer jusqu'en 2018
   DOAJ
IF 4.011
TC 23
UR https://archimer.ifremer.fr/doc/00454/56540/58246.pdf
   https://archimer.ifremer.fr/doc/00454/56540/58247.xlsx
   https://archimer.ifremer.fr/doc/00454/56540/58248.pdf
LA English
DT Article
AB Bonamia ostreae has been associated with the decline of flat oyster Ostrea edulis populations in some European countries. This obligatory intracellular parasite persists and multiplies into hemocytes. Previous in vitro experiments showed that apoptosis is activated in hemocytes between 1 h and 4 h of contact with the parasite. The flat oyster uses the apoptosis pathway to defend against B. ostreae. However, the parasite might be also able to modulate this response in order to survive in its host. In order to investigate this hypothesis the apoptotic response of the host was evaluated using flow cytometry, transmission electron microscopy and by measuring the response of genes involved in the apoptotic pathway after 4 h. In parallel, the parasite response was investigated by measuring the expression of B. ostreae genes involved in different biological functions including cell cycle and cell death. Obtained results allow describing molecular apoptotic pathways in O. edulis and confirm that apoptosis is early activated in hemocytes after a contact with B. ostreae. Interestingly, at cellular and molecular levels this process appeared downregulated after 44 h of contact. Concurrently, parasite gene expression appeared reduced suggesting that the parasite could inhibit its own metabolism to escape the immune response. 
PY 2018
PD AUG
SO Scientific Reports
SN 2045-2322
PU Nature Publishing Group
VL 8
IS 1
UT 000442276600010
DI 10.1038/s41598-018-29776-x
ID 56540
ER

EF