The role of the nuclease, HARBI1-like
protein (mjHARBI1-like) in the innate immunity of Marsupenaeus japonicus was explored in this study. The 1361 bp
cDNA sequence of mjHARBI1-like was cloned from M. japonicus using RACE. RT-qPCR analysis results showed that the gills and hepatopancreas of M. japonicus were the main tissues where mjHARBI1-like is expressed. In addition, it was also found that white spot syndrome virus (WSSV) or Vibrio alginolyticus challenge could stimulate mjHARBI1-like expression. After mjHARBI1-likewas inhibited, expression of immune genes such as toll, p53,
myosin, and proPO were significantly downregulated (P < 0.01). However, in shrimp hemocytes,
hemocyanin and
tumor necrosis factor-α (TNF-α) were up-regulated significantly (P < 0.01). This study demonstrated that mjHARBI1-like plays a key role in the progression of WSSV and V. alginolyticus
infection. Specifically, the cumulative mortality of WSSV-infected and V. alginolyticus-infected shrimp was significantly advanced by double-strand RNA interference (dsRNAi) of mjHARBI1-like. Apoptosis studies indicated that mjHARBI1-dsRNA treatment caused a reduction in hemocyte apoptosis in bacterial and viral groups. In addition, phagocytosis experiments illustrated that mjHARBI1-dsRNA treatment led to a lower phagocytosis rate in hemocytes of V. alginolyticus-challenged shrimp. It was also found that knockdown of mjHARBI1-like inhibited shrimp
phenoloxidase (PO) activity,
superoxide dismutase (SOD) activity, and total hemocyte count (
THC) after WSSV or V. alginolyticus
infection. These data indicate a regulative role of mjHARBI1-likein the immunity of shrimp in response to pathogen
infection. Resultantly, it was concluded that mjHARBI1-like might have a positive effect on the anti-WSSV immune response of shrimp by regulating apoptosis,
THC, PO activity, and SOD activity. Additionally, mjHARBI1-like might promote anti-V. alginolyticus
infection by participating in regulating phagocytosis, apoptosis, SOD activity, PO activity, and
THC.