Flightless-I (FliI) is a potential negative regulator of the Toll pathway in Litopenaeus vannamei. Issue 2 (February 2015)

• Record Type: Journal Article
• Authors: Zhang, Shuang; Qiu, Wei; Chen, Yong-gui; Yuan, Feng-Hua; Li, Chao-Zheng; Yan, Hui; Weng, Shao-Ping; He, Jian-Guo
• Is Part Of: Fish & shellfish immunology. Volume 42:Issue 2(2015:Feb.)
• Page Start: 413
• Page End: 425
• Publication Date: 2015-02
• Subjects: Fishes -- Immunology -- Periodicals; Shellfish -- Immunology -- Periodicals; Poissons -- Immunologie -- Périodiques; Crustacés -- Immunologie -- Périodiques; 571.9617
• DOI: 10.1016/j.fsi.2014.10.023
• Languages: English
• ISSNs: 1050-4648

Abstract

<abstract xml:lang="en" abstract-type="author" id="abs0010"> <title id="sectitle0010">Abstract</title> <sec> <p id="abspara0010">Flightless-I (FliI) is a protein negatively modulates the Toll-like receptor (TLR) pathway through interacting with Myeloid differentiation factor 88 (MyD88). To investigate the function of FliI in innate immune responses in invertebrates, <italic>Litopenaeus vannamei</italic> FliI (LvFliI) was identified and characterized. The full-length cDNA of LvFliI is 4, 304 bp long, with an open reading frame (ORF) encoding a putative protein of 1292 amino acids, including 12 leucine-rich repeat (LRR) domains at the N-terminus and 6 gelsolin homology (GEL) domains at the C-terminus. The LvFliI protein was located in the cytoplasm and LvFliI mRNA was constitutively expressed in healthy <italic>L. vannamei</italic>, with the highest expression level in the muscle. LvFliI could be up-regulated in hemocytes after lipopolysaccharide (LPS), poly I:C, CpG-ODN2006, <italic>Vibrio parahaemolyticus</italic>, <italic>Staphylococcus aureus</italic>, and white spot syndrome virus (WSSV) challenges, suggesting a stimulation response of LvFliI to bacterial and immune stimulant challenges. Upon LPS stimulation, overexpression of LvFliI in <italic>Drosophila</italic> Schneider 2 cells led to downregulation of <italic>Drosophila</italic> and shrimp antimicrobial peptide (AMP) genes. Knockdown of LvFliI by RNA interference (RNAi) resulted in an increase of the expression of three shrimp AMP genes (PEN2, crustin, and Lyz1). However, the mortality rates of LvFliI-knockdown shrimp in response to <italic>V</italic>. <italic>parahaemolyticus</italic>, <italic>S</italic>. <italic>aureus</italic> or WSSV infections were not significantly different from those of the control group. Taken together, all the results suggested that LvFliI may play a negative role in TLR signaling response in <italic>L. vannamei</italic>.</p> </sec> </abstract>