AQUA 2024

August 26 - 30, 2024

Copenhagen, Denmark

EFFECTS OF PmSTAT AND PmSOCS2 KNOCKDOWN ON WHITE SPOT SYNDROME VIRUS INFECTION IN Penaeus monodon

Kuakarun Krusong *, Thapanan Jatuyosporn, Pasunee Laohawutthichai, Fernanda Cornejo-Granados , Luigui Gallardo-Becerra , Filiberto Sánchez Lopez, Anchalee Tassanakajon and Adrián Ochoa-Leyva

Center of Excellence in Structural and Computational Biology, Department of Biochemistry, Faculty of Science, Chulalongkorn University, Bangkok 10330, Thailand

Kuakarun.K@chula.ac.th

 



 White spot syndrome virus (WSSV) is a lethal pathogen that causes 100% mortality within 3-7 days after infection.  Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway play a role during WSSV infection.  Previous work has shown that PmDOME and PmSTAT silencing in black tiger shrimp (Penaeus monodon ) reduced WSSV copy numbers and delayed the cumulative mortality. In this work,  the next-generation sequencing (NGS) was performed using STAT-silenced shrimp,  WSSV-infected STAT-silenced shrimp and  WSSV-infected shrimp.  Transcriptome data showed that a total of differential expression genes  (DEGs) of WSSV infection was 675, while 138 up-regulated genes were from STAT-silencing + WSSV .  Ten genes were randomly selected and their expression levels were verified by qRT-PCR.  In addition,  the  roles of PmSOCS2, a JAK/STAT inhibitor, were also investigated. Silencing of PmSOCS2  significantly affected the expression of ProPO2 , ALFPm3 , Penaeidin 3 , CrustinPm1 and CrustinPm7. This work emphasizes the importance of the JAK/STAT signaling pathway during WSSV infection.