In:
Scientific Reports, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2019-09-17)
Abstract:
White spot syndrome virus (WSSV) is one of the most lethal viruses severely affecting shrimp industry. This disease can cause 100% mortality of farmed shrimp within a week. This work aims to characterize clathrin assembly proteins in Penaeus monodon and investigate their roles in WSSV entry. In general, clathrin assembly proteins form complexes with specific receptors and clathrins, leading to clathrin-mediated endocytosis. Adaptor protein 2 (AP-2), which is responsible for endocytosis at plasma membrane, consists of four subunits including α, β2, μ2 and σ2. Knockdown of clathrin coat AP17, or σ subunit of AP-2 dramatically reduced WSSV infectivity. Similar results were observed, when shrimp were pre-treated with chlorpromazine (CPZ), an inhibitor of clathrin-dependent endocytosis. The complete open reading frames of AP-2β and μ subunits of P . monodon are reported. Pm AP-2 β was up-regulated about 4-fold at 6 and 36 h post-WSSV infection. Knockdown of Pm AP-2β delayed shrimp mortality during WSSV infection, of which WSSV intermediate early 1 gene expression was also down-regulated. Immunogold-labelling and transmission electron microscopy revealed that Pm AP-2β co-localized with WSSV particles at plasma membrane. In addition, Pm AP-2β-silencing significantly affected the expression levels of Pm STAT, Pm DOME, Pm Dorsal and ALF Pm 3 during WSSV infection. It is possible that Pm AP-2β is associated with the JAK/STAT and the Toll pathway.
Type of Medium:
Online Resource
ISSN:
2045-2322
DOI:
10.1038/s41598-019-49852-0
Language:
English
Publisher:
Springer Science and Business Media LLC
Publication Date:
2019
detail.hit.zdb_id:
2615211-3
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