Shrimp SIRT1 activates of the WSSV IE1 promoter independently of the NF-κB binding site

Zi Ning Kao, Chun Hung Liu, Wang Jing Liu, Ramya Kumar, Jiann Horng Leu, Han Ching Wang

Research output: Contribution to journalArticlepeer-review

Abstract

Since the mechanisms by which cellular factors modulate replication of the shrimp viral pathogen white spot syndrome virus (WSSV) are still largely unknown, here we consider the sirtuins, a family of NAD+-dependent protein deacetylases that are known to function as regulatory factors that activate or suppress viral transcription and replication in mammals. In particular, we focus on SIRT1 by isolating and characterizing LvSIRT1 from white shrimp (Litopenaeus vannamei) and investigating its involvement in WSSV infection. DsRNA-mediated gene silencing led to the expression of WSSV genes and the replication of genomic DNAs being significantly decreased in LvSIRT1-silenced shrimp. The deacetylase activity of LvSIRT1 was significantly induced at the early stage (2 hpi) and the genome replication stage (12 hpi) of WSSV replication, but decreased at the late stage of WSSV replication (24 hpi). Treatment with the SIRT1 activator resveratrol further suggested that LvSIRT1 activation increased the expression of several WSSV genes (IE1, VP28 and ICP11). Lastly, we used transfection and dual luciferase assays in Sf9 insect cells to show that while the overexpression of LvSIRT1 facilitates the promoter activity of WSSV IE1, this enhancement of WSSV IE1 expression is achieved by a transactivation pathway that is NF-κB-independent.

Original languageEnglish
Pages (from-to)910-919
Number of pages10
JournalFish and Shellfish Immunology
Volume106
DOIs
Publication statusPublished - 2020 Nov

All Science Journal Classification (ASJC) codes

  • Environmental Chemistry
  • Aquatic Science

Fingerprint Dive into the research topics of 'Shrimp SIRT1 activates of the WSSV IE1 promoter independently of the NF-κB binding site'. Together they form a unique fingerprint.

Cite this