摘要：Yellow head virus (YHV) is a pathogen which causes high mortality in penaeid shrimp. Previous studies suggested that YHV enters shrimp cells via clathrin-mediated endocytosis. This research investigated the roles of clathrin adaptor protein 2 subunit β (AP-2β) from
Penaeus monodon during YHV infection.
PmAP2-β was continuously up-regulated more than twofold during 6–36 hpi. Suppression of
PmAP2-β significantly reduced YHV copy numbers and delayed shrimp mortality. Quantitative RT-PCR revealed that knockdown of
PmAP2-β significantly enhanced the expression level of
PmSpätzle, a signaling ligand in the Toll pathway, by 30-fold at 6 and 12 hpi. Moreover, the expression levels of gene components in the Imd and JAK/STAT signaling pathways under the suppression of
PmAP2-β during YHV infection were also investigated. Interestingly, anti-lipopolysaccharide factor isoform 3 (ALF
Pm3) was up-regulated by 40-fold in
PmAP2-β knockdown shrimp upon YHV infection. In addition, silencing of
PmAP2-β dramatically enhanced crustin
Pm1 expression in YHV-infected shrimp. Knockdown of ALF
Pm3 and crustin
Pm1 significantly reduced shrimp survival rate. Taken together, this work suggested that
PmAP2-β-deficiency promoted the Toll pathway signalings, resulting in elevated levels of ALF
Pm3 and crustin
Pm1, the crucial antimicrobial peptides in defence against YHV.
