FN Archimer Export Format PT J TI Transcriptomic analysis of clam extra pallial fluids reveals immunity and cytoskeleton alterations in the first week of Brown Ring Disease development BT AF Rahmani, Alexandra Corre, Erwan Richard, Gaëlle Bidault, Adeline Lambert, Christophe Oliveira, Louisi Thompson, Cristiane Thompson, Fabiano Pichereau, Vianney Paillard, Christine AS 1:1;2:2;3:1;4:1;5:4;6:3;7:3;8:3;9:1;10:4; FF 1:;2:;3:;4:;5:;6:;7:;8:;9:;10:; C1 Univ Brest, CNRS, IRD, Ifremer, UMR 6539 LEMAR, F-29280, Plouzane, France Sorbonne Universités, Université Pierre et Marie Curie-Paris 6, CNRS, FR2424, Station Biologique de Roscoff, Roscoff, France Centro de Ciências da Saúde, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil Univ Brest, CNRS, IRD, Ifremer, UMR 6539 LEMAR, F-29280, Plouzane, France C2 UBO, FRANCE UNIV PARIS 06, FRANCE UNIV FED RIO DE JANEIRO UFRJ, BRAZIL CNRS, FRANCE UM LEMAR IN WOS Cotutelle UMR copubli-france copubli-int-hors-europe copubli-sud IF 1.618 TC 5 UR https://archimer.ifremer.fr/doc/00510/62131/66362.pdf LA English DT Article DE ;Brown ring disease;V. tapetis;R. philippinarum;Hemocytes;Actin cytoskeleton;beta-Thymosin;Coactosin;Resting cells AB The Brown Ring Disease is an infection caused by the bacterium Vibrio tapetis on the Manila clam Ruditapes philippinarum. The process of infection, in the extrapallial fluids (EPFs) of clams, involves alteration of immune functions, in particular on hemocytes which are the cells responsible of phagocytosis. Disorganization of the actin-cytoskeleton in infected clams is a part of what leads to this alteration. This study is the first transcriptomic approach based on collection of extrapallial fluids on living animals experimentally infected by V. tapetis. We performed differential gene expression analysis of EPFs in two experimental treatments (healthy-against infected-clams by V. tapetis), and showed the deregulation of 135 genes. In infected clams, a downregulation of transcripts implied in immune functions (lysosomal activity and complement- and lectin-dependent PRR pathways) was observed during infection. We also showed a deregulation of transcripts encoding proteins involved in the actin cytoskeleton organization such as an overexpression of β12-Thymosin (which is an actin sequestration protein) or a downregulation of proteins that closely interact with capping proteins such as Coactosin, that counteract action of capping proteins, or Profilin. We validated these transcriptomic results by cellular physiological analyses that showed a decrease of the lysosome amounts and the disorganization of actin cytoskeleton in infected hemocytes. PY 2019 PD OCT SO Fish & Shellfish Immunology SN 1050-4648 PU Elsevier BV VL 93 UT 000488998300105 BP 940 EP 948 DI 10.1016/j.fsi.2019.08.025 ID 62131 ER EF