The MIP-T3 from shrimp Litopenaeus vannamei restricts white spot syndrome virus infection via regulating NF-κB activation

In vertebrate, MIP-T3 (microtubule-interacting protein associated with TRAF3) functions as a regulator of innate immune response that involves many cellular processes. However, the immune response regulated by shrimp (an arthropod) MIP-T3 remains unrevealed. In the present study, a MIP-T3 homolog from shrimp Litopenaeus vannamei (named as LvMIP-T3) was cloned and identified. LvMIP-T3 had a 2076 bp open reading frame (ORF), encoding a polypeptide of 691 amino acids that contained a classic coiled-coil domain in the C-terminal that showed a high degree of conservation to other homologs. LvMIP-T3 could interact with LvTRAF6, a member of the canonical NF-kappa B pathway, but not LvTRAF3, which implies that LvMIP-T3 is able to regulate NF-kappa B activity via its interaction with LvTRAF6. In addition, LvMIP-T3 was substantially inducted in response to white spot syndrome virus (WSSV) challenge, and we demonstrated that LvMIP-T3 facilitated the expression of NF-kappa B-mediated several Penaeidins (antimicrobial peptides, AMPs) to oppose infection. Taken together, we identified a MIP-T3 homolog from shrimp L. vannamei that played a positive role in the TRAF6/NF-kappa B/AMPs axis mediated defense response, which will contribute to better understand the regulator relationship among members of the canonical NF-kappa B pathway in shrimp, and provides some insights into disease resistance breeding.

Automated summary

In this study, a MIP-T3 homolog from shrimp Litopenaeus vannamei was cloned and identified. The LvMIP-T3 played a positive role in the TRAF6/NF-kappa B/AMPs axis-mediated defense response and facilitated the expression of antimicrobial peptides to oppose infection.