Identification of a LPS-induced TNF-α factor (LITAF) from mollusk Solen grandis and its expression pattern towards PAMPs stimulation

Fish Shellfish Immunol. 2013 Oct;35(4):1325-8. doi: 10.1016/j.fsi.2013.07.034. Epub 2013 Jul 26.

Abstract

Lipopolysaccharide-induced TNF-α factor (LITAF) is one of the most important transcription factors mediating TNF-α transcription. In the present study, a LITAF gene (designated as SgLITAF) was identified from razor clams Solen grandis. The full-length cDNA of SgLITAF was of 1476 bp, encoding a polypeptide of 130 amino acids showed high similarity to other known LITAFs. SgLITAF encoded a LITAF domain and the Zn(2+)-binding motifs in the domain were well conserved. The mRNA transcripts of SgLITAF were detected in all tested tissues of healthy razor clams, including mantle, gill, gonad, hemocytes, muscle and hepatopancreas, and with the highest expression level in hepatopancreas. The expression level of SgLITAF in hemocytes was significantly up-regulated (P < 0.01) after razor clams were stimulated by LPS or β-1, 3-glucan, but no obvious fluctuation of SgLITAF mRNA expression was observed after PGN stimulation. All the results indicated that there might be a LITAF-regulated TNF-α signaling pathway existing in S. grandis, which involved in the immune response not only against gram-negative bacteria but also towards fungi.

Keywords: Innate immunity; LITAF; Real-time PCR; Solen grandis; Transcription factor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bivalvia / genetics*
  • Bivalvia / immunology*
  • Bivalvia / metabolism
  • DNA, Complementary / genetics
  • DNA, Complementary / metabolism
  • Expressed Sequence Tags
  • Gene Expression Regulation
  • Lipopolysaccharides / pharmacology
  • Molecular Sequence Data
  • Organ Specificity
  • Protein Structure, Tertiary
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Real-Time Polymerase Chain Reaction
  • Sequence Analysis, DNA
  • Sequence Analysis, Protein
  • Sequence Homology
  • Tumor Necrosis Factor-alpha / genetics*
  • Tumor Necrosis Factor-alpha / metabolism
  • beta-Glucans / pharmacology

Substances

  • DNA, Complementary
  • Lipopolysaccharides
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • beta-Glucans
  • beta-1,3-glucan

Associated data

  • GENBANK/JN642122