Abstract
Flagellin is a key bacterial virulence factor that can stimulate molecular immune signaling in both animals and plants. The detailed mechanisms of recognizing flagellin and mounting an efficient immune response have been uncovered in vertebrates; however, whether invertebrates can discriminate flagellin remains largely unknown. In the present study, the homolog of human SHOC2 leucine rich repeat scaffold protein in kuruma shrimp (Marsupenaeus japonicus), designated MjShoc2, was found to interact with Vibrio anguillarum flagellin A (FlaA) using yeast two-hybrid and pull-down assays. MjShoc2 plays a role in antibacterial response by mediating the FlaA-induced expression of certain antibacterial effectors, including lectin and antimicrobial peptide. FlaA challenge, via MjShoc2, led to phosphorylation of extracellular regulated kinase (Erk), and the subsequent activation of signal transducer and activator of transcription (Stat), ultimately inducing the expression of effectors. Therefore, by establishing the FlaA/MjShoc2/Erk/Stat signaling axis, this study revealed a new antibacterial strategy in shrimp, and provides insights into the flagellin sensing mechanism in invertebrates.
Highlights
Many bacterial species have a flagellum [1]
We revealed that extracellular regulated kinase (Erk) phosphorylation occurred downstream of flagellin A (FlaA)/MjShoc2, and led to signal transducer and activator of transcription (Stat) activation, resulting in transcription of certain effectors
V. anguillarum FlaA was used as the bait to screen a Gateway AD yeast two-hybrid library derived from kuruma shrimp to identify the proteins that bind flagellin
Summary
Flagellum contributes to bacterial pathogenesis by participating in multiple stages throughout the infection process, including adherence and colonization, biofilm development, secretion of other virulence effectors, further penetration through tissues, and modulation of host immune responses [2,3]. Mutation of flagellin A (FlaA) of the NB10 strain led to a 50% decrease in motility and a 700-fold decrease in the bacteria’s infection ability, while deletion of FlaD or FlaE did not alter motility, but suppressed the pathogenicity markedly [5,6]. These data suggested the multifactorial involvement of flagellins in V. anguillarum virulence. Sensing flagellin and initiating immune responses could be an effective strategy to resist infection
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